Abstract
Breast cancer is the most common neoplasm in women, and it is a rare cancer in men. A handful of occupational exposures, including ethylene oxide and shift work that involve circadian disruption, have been linked, with limited human evidence, to an increased risk of breast cancer in women. Evidence is still being gathered regarding other occupational and environmental exposures, such as several hydrocarbons and certain components of air pollution, that are suspected to play an etiologic role. Therapeutic exposure to several medications and to X-radiation and γ-radiation has been linked with sufficient evidence to female breast cancer; however, the weight of occupational evidence for these same carcinogens is still deemed limited or insufficient. Between 2 and 5% of the breast cancers diagnosed now are estimated to be attributable to occupational exposures; as the most common cancer among women, breast cancer thus represents an important burden on our societies. Although no occupational exposures have yet been linked specifically to male breast cancer, similarities between male and female breast cancers suggest potential common causal factors. As only about 30% of new cases of breast cancer can be explained by known risk factors, continued research on the relationship between environmental and occupational exposures and breast cancer is warranted.
Access provided by Autonomous University of Puebla. Download chapter PDF
Similar content being viewed by others
Keywords
Female Breast Cancer
Descriptive Epidemiology
Breast cancer is the most common malignancy affecting women. Indeed, among all cancers affecting women, breast cancer has the highest incidence and mortality, in more developed and less developed countries. In 2018, 2.09 million new cases were reported in the world, corresponding to 24.2% of all cancers occurring in women that year. The incidence rates of female breast cancer vary greatly, being highest among women in North America, Southern, Western, and Northern Europe, and Australia and New Zealand (greater than 80 new cases annually per 100,000 women). Incidence is lowest in South-Central Asia, and in Eastern and Middle Africa (incidence below 30 new cases annually per 100,000 women). The range of mortality rates for female breast cancer is narrower than that of incidence rates, due to better survival in more developed countries as compared to less developed countries (Fig. 24.1) [1].
Age-standardized incidence and mortality rates of female breast cancer in different world regions. GLOBOCAN 2018 (W: Standardization done according to the average-age structure of the world) (Ferlay J, Ervik M, Lam F, Colombet M, Mery L, Piñeros M, Znaor A, Soerjomataram I, Bray F (2018). Global Cancer Observatory: Cancer Today. Lyon, France: International Agency for Research on Cancer. Available from: https://gco.iarc.fr/today, accessed [16 March 2019])
Incidence rates have been decreasing in North America, a few European countries and Australia and New Zealand, but are currently increasing in less developed countries. In the United States, the decrease in incidence rates over the last few years has been attributed to the reduction of large-scale hormone replacement therapy prescription [2, 3]. Secular time trends in mortality rates have generally been more stable than those of incidence and have, in fact, decreased particularly in more developed countries [4].
General Epidemiology and Lifestyle-Related Risk Factors
As is the case for most cancers, breast cancer is a multifactorial disease. Several nonoccupational factors have been found to be consistently associated with increased risks of developing breast cancer; a selection of these is presented in Table 24.1.
Reproductive Factors
Early age at menarche (≤11 vs. ≥15 years, 1.1–1.9-fold increased risk) [5, 6], late age at menopause (≥55 vs. ≤45 years, 1.1–1.9-fold increased risk) [5, 6], nulliparity (nulliparous vs. parous women: one to twofold increase in risk, inconclusive after one full-term pregnancy) [7], and age at first full-term pregnancy above 30 years (one to twofold increased risk compared to women with first full-term pregnancy <20 years of age) [6,7,8,9,10,11] have been consistently associated with an increased risk of breast cancer. Breastfeeding reduces risk in both pre- and postmenopausal women [14, 19]; a pooled analysis showed a decreased risk of 4% for every 12 months a woman breastfeeds, regardless of whether a woman breastfeeds in consecutive children or not [12].
Use of Exogenous Hormones
According to the International Agency for Research on Cancer (IARC), diethylstilbestrol may cause breast cancer in women exposed during pregnancy [13]. The use of oral contraceptives comprising estrogen and progestogen among current and recent users only is also associated with an increased risk of developing breast cancer in young women [13]; the risk is particularly increased among women with benign breast disease who use oral contraceptives, and among women who used oral contraceptives either before 20 years of age (relative risk ~2.1) or before their first full-term pregnancy (relative risk ~1.6) [6, 7, 13]. The use of hormone replacement therapy containing estrogen and progestogen also increases the risk of developing breast cancer (relative risk <2 for women who took them for several years or in high doses), as does hormone replacement therapy containing estrogen only [6, 7, 13, 15].
Diet, Body Size, and Physical Activity
The World Cancer Research Fund [14] evaluated the available evidence on the risk of cancer and several aspects of diet, physical activity, and body size. The IARC Handbooks of Cancer Prevention series also included similar evaluations [16, 17]. The results from the World Cancer Research Fund and IARC are of major importance and are summarized below.
There is evidence suggesting that total fat consumption may be associated with the risk of developing postmenopausal breast cancer, but the relationship has not been clearly established [14]. Regarding body fatness, an international panel of experts judged the evidence that supports an exposure–response relationship convincing for postmenopausal women, whereas the same group judged probable a protective effect among premenopausal women [11, 16]. There is robust evidence for a mechanistic explanation indicating that greater body adiposity after menopause is associated with tissue inflammation, which may play a part in initiation or promotion of cancer [14, 17]. According to the evaluation of the World Cancer Research Fund, increased abdominal fat is associated with increased risk of developing postmenopausal breast cancer (relative risk 1.19, 95% confidence interval [CI] 1.10–1.28 per 0.1 increment in waist-to-hip ratio), as is weight gain in adults (relative risk 1.05, 95% CI 1.04–1.07 per 5 kg gained), whereas higher birth weight is associated with an increased risk of premenopausal breast cancer (relative risk 1.08, 95% CI 1.04–1.13) [14].
With respect to height, prospective epidemiological studies show a clear exposure–response relationship, and there is some evidence for plausible mechanisms in humans. The World Cancer Research Fund considers that there is convincing evidence that factors that lead to greater adult attained height (relative risk 1.03, 95% CI 1.01–1.04 per 5 cm increase) are associated with increased incidence among both pre- and postmenopausal women [14].
Evidence from prospective studies on physical activity suggests a protective effect against both pre- and postmenopausal breast cancer for high levels of physical activity, including occupational active employment [20] but no evidence that breast cancer risk is increased with inactivity, except in relation to occupational sedentariness for which increased risks of about 20% has been reported [21]. The evidence is stronger for postmenopausal breast cancer than for premenopausal breast cancer. There are little data regarding frequency, duration, or intensity of activity, but the evidence is robust for mechanisms operating in humans [14, 16].
Alcoholic Beverages
In agreement with the IARC evaluation, which considered alcohol as carcinogenic (Group 1 agent) to the human breast [22], the World Cancer Research Fund also classified the evidence as “convincing” that consumption of alcoholic beverages increases incidence in both pre- and postmenopausal breast cancer, irrespective of the type of alcoholic beverage (i.e., no difference between wine, beer, liquor). An exposure–response relationship is apparent: all studies in which an exposure gradient was investigated found that risks increased with increasing alcohol consumption (relative risk 1.10, 95% CI 1.06–1.14 per 10 g/day increase) [14].
Tobacco Smoking
The IARC considers that there is limited evidence suggesting that tobacco smoking may be associated with increasing incidence of breast cancer, in particular risk appears to increase when smoking starts early and before a woman’s first full-term pregnancy (before the breast tissue matures) and if it continues for several decades [22].
Ionizing Radiation
The IARC classified X-radiation and γ-radiation as carcinogenic agents with sufficient evidence in humans in relation to developing breast cancer (two- to fourfold increase in risk for high doses compared to minimal exposure; risk may be higher when exposure occurs between puberty and childbearing years, when breast tissue is still proliferating) [7, 18, 23]. The evidence on which the evaluation was based emanates from many studies in special populations, such as atomic bomb survivors, medical patients, and women who were exposed in utero (offspring of atomic bomb survivors and pregnant medical patients) (see Table 24.1) [18, 23, 24]. In addition, α-radiation and neutrons have been classified as carcinogenic agents for several cancer sites, but the evidence is deemed insufficient for female breast [18].
Family History of Breast Cancer and Genetic Factors
Family history of breast cancer increases a woman’s risk substantially depending on the age at which affected relatives were diagnosed, as well as the age of the woman herself, the number of affected relatives, and the generational distance between the relatives and the woman. The familial relative risk (FRR) for first-degree relatives of breast cancer patients is about twice that of women without a family history of breast cancer [25, 26] and increases more than fourfold for women who have a first-degree relative with premenopausal bilateral breast cancer or who have two first-degree relatives with any form of breast cancer [5,6,7,8,9,10,11, 27, 28]; most of this FRR appears to be due to inherited susceptibility [26, 29, 30].
Several important genetic variants have been found, ranging from high-penetrance but rare mutations that confer very high risks (ranging from 5 to more than 20), moderate-penetrance mutations that are associated with risks between 1.5 and 5, and low-penetrance but frequent polymorphisms associated with lower risks (see Table 24.2) [28, 31]. Based on recent evidence, it appears that genetic susceptibility is involved in a large proportion of breast cancer cases. According to a polygenic model, about half of all breast cancer cases arise in a small, highly susceptible subgroup comprising about 12% of women (those with a risk above 10% by age 70 years). In fact, half of the female population has a breast cancer risk of only 3% or less, accounting for about 12% of all breast cancer cases [32].
About 25% of the FRR is explained by high-risk alleles such as BRCA1, BRCA2, PTEN, and TP53. When the rare intermediate-risk alleles (CHEK2, ATM, BRIP1, PALB2) are also considered, another 2–3% of the FRR is accounted for (see Table 24.2) [33]. In addition to these high- and intermediate-risk alleles, genetic studies have identified 19 common low-risk susceptibility alleles that explain yet another 10% of the FRR [34,35,36,37,38,39,40,41,42,43]. Many of these genes are involved in DNA repair mechanisms (see Table 24.2) [28].
In summary, the known susceptibility alleles account for only about one-third of the overall FRR. Recent genome-wide linkage studies did not identify any additional rare variants that confer large breast cancer risks (relative risk >2) [28]. Thus, the remainder of the FRR could likely be explained by some combination of common variants although certain authors consider that including newly discovered common variants would only modestly improve the performance of risk models for breast cancer [44].
Occupational Exposures
The IARC Monographs on the Evaluation of Carcinogenic Risks to Humans series is recognized worldwide as a dependable source to identify carcinogenic agents and circumstances. Agents are classified into one of the five groups: Group 1 agents are deemed to be carcinogenic to humans; Group 2A agents probably carcinogenic to humans; Group 2B agents possibly carcinogenic to humans; Group 3 agents not classifiable as to their carcinogenicity to humans; and Group 4 agents probably not carcinogenic to humans [45]. The evidence considered by the working groups to classify the agents comes mainly from human and animal studies. Thus, some agents may be classified as carcinogenic to humans if there is sufficient evidence in humans, or limited evidence in humans but sufficient evidence in animals. Finally, an agent can be considered carcinogenic to a certain organ, but not necessarily to another one. Table 24.3 shows the known or suspected causes of breast cancer abstracted from the IARC Monographs [46].
According to the different IARC Working Groups, the existing Group 1 agents with sufficient evidence of carcinogenicity to the human breast are not related to occupational exposures. For example, the available evidence for alcoholic beverages, diethylstilbestrol, and combined estrogen-progestogen oral contraceptives or hormone replacement therapy is derived from personal use, and not from exposures in occupational settings. The rationale presented for X-radiation and γ-radiation is derived from studies carried out on atomic bomb survivors and women who underwent radiation therapy before menopause (for conditions such as acute postpartum mastitis, benign breast disease, and follow-up of tuberculosis by chest fluoroscopies) although a few occupational studies have also shown increased risks among exposed workers [18]. The evidence for polychlorinated biphenyls (PCBs) comes from both nonoccupational and occupational exposures [47]. Only one Group 1 agent, ethylene oxide, is an occupational exposure. However, evidence for carcinogenicity to the human breast is limited for this exposure. It is important to appreciate that few studies of occupational risk factors for breast cancer have been carried out, so the paucity of well-established occupational carcinogens may be due to lack of research.
Estrogen-only hormone replacement therapy and active tobacco smoking have been classified by the IARC as probably carcinogenic to the human female breast, with limited evidence in humans, but again, these exposures are not considered to be related to occupation.
Occupational Agents with Limited Evidence for Carcinogenicity to the Human Breast
Ethylene oxide (Group 1 agent) [48] and night shift work (Group 2A agent) [49] are considered to be related to occupation (see Table 24.4).
Ethylene Oxide
Ethylene oxide is used mainly as a raw material for the production of several industrial chemicals, including glycols, which are used in the production of a number of consumer goods [65]. Less than 1% is used as a sterilizing agent, a fumigant, or a pesticide by different healthcare facilities, spice manufacturers, or sterilization contractors [65]. In the early 2000s, the approximate estimates of the number of exposed workers in the United States were in the order of 48,000 [66]. In the European Union in the early 1990s, the corresponding estimate was around 47,000 workers [67].
The data used by the IARC to classify ethylene oxide [48] is derived mainly from four occupational cohort studies [50,51,52,53,54]. Because mortality from breast cancer is highly misclassified, one must rely on incidence rates, as reported in three of the four aforementioned cohort studies [50,51,52, 54]. A US National Institute for Occupational Safety and Health cohort study of 7500 women [52], which had accounted for several important potential confounding variables, showed a clear exposure–response relationship between exposure to ethylene oxide and the incidence of breast cancer, with a relative risk of 1.87 among women in the highest quintile of cumulative exposure as compared to the lowest quintile. A smaller study from the United States also showed increased risks (standardized morbidity ratios 1.57–1.72) among women from a sterilization company [51]. In a Swedish study, no increase in risk was initially found [50], but an internal analysis after a longer follow-up revealed significantly increased risks for women in the two upper quartiles of exposure compared to the lower half of exposure (rate ratios of 2.76 and 3.55) [54]. A few animal studies showed increased risks of mammary tumors in rodents. Additional mechanistic studies showed alkylation, gene mutations, and chromosomal alterations following binding to cellular macromolecules resulting in DNA, RNA, and protein (including hemoglobin) adducts; these led the IARC Working Group to classify ethylene oxide as carcinogenic to humans (Group 1 agent) but with limited human evidence for breast cancer and lymphoid tumors [48].
Night Shift Work
Although shift work corresponds to several definitions of work schedules, including hours other than the traditional daytime work period [68], it is generally considered as “…the organization of working time by different teams in succession to cover more than the usual 8-h day, up to and including the whole 24-h period” [69]. Shift work disrupts biological rhythms and the most important factor appears to be the proportion of time worked at night [70, 71]. The industrial sectors with the largest percentages of workers on a non-daytime shift are accommodation and food services, agriculture, health services, and transportation and communication [72]. It was estimated in 2005 that 9–30% of workers in the European Union, depending on the country, worked shifts that included night work [73]; in 2004 that proportion was estimated to be about 15% in the United States [74].
The IARC Working Group cited data from eight studies designed specifically to evaluate the relationship between shift work involving night work and the risk of breast cancer [49]. Six of these studies reported a modest increase in risk (generally less than twofold) among women who worked night shifts for a long period of time, or who did rotating work including night shifts as compared to women who worked daytime hours. Several definitions of shift work were used as well as different designs: two prospective cohort studies among nurses [55, 56]; three nested case-control studies [59,60,61]; and one retrospective case-control study [62]. Two studies showed negative results, a census-based cohort study [57] with important design limitations, and a case-control study initially designed to study the relationship between electromagnetic fields and breast cancer [63]. These studies included mainly white women and women with postmenopausal breast cancer. In some of the studies, not all potential confounding variables were accounted for. Misclassification of exposure may have biased the results toward the null. Studies of aircraft personnel were considered by the IARC Working group to support the association between shift work and breast cancer although these workers had concomitant exposures that could have confounded the association (such as cosmic radiation and electromagnetic fields) [49].
Since the IARC evaluation, several additional studies, including five cohort studies [58, 75,76,77,78] and eleven case-control studies [64, 79,80,81,82,83,84,85,86,87,88,89] have been published on shift work in relation to breast cancer risk. Most of these studies have been reviewed in 2016 by an expert working group of the French Agency for Food, Environmental and Occupational Health & Safety (ANSES). The working group concluded that these recent epidemiological studies provide more evidence on the increased risk of breast cancer among night shift workers; however, this evidence is still limited and it is not yet possible to rule out, with certainty, the existence of residual confounding factors that could explain some of the observed associations [90, 91].
Seven recent meta-analyses [92,93,94,95,96,97,98] reported at least one meta-risk estimate of breast cancer in association with night shift work based on slightly different sets of studies. Overall, meta-risk estimates ranged from 0.99 (ten prospective studies [98]) to 1.40 (nine high-quality studies [93]) for ever/never night shift work exposure. These meta-analyses were not conclusive on other metrics of night shift work exposure or other study characteristics.
The main theory underlying the detrimental effects of shift work is that light at night can disrupt circadian rhythms through its effect on melatonin synthesis and on the circadian gene function of the suprachiasmatic nucleus. This disruption might increase cancer risk through several pathways [99], including a decrease of melatonin’s possible oncostatic and free radical scavenging properties, as well as perturbations of the involvement of circadian genes in cell proliferation, apoptosis, cell cycle control, and DNA–damage response [49]. A case-control study nested in a cohort of nurses reported an inverse relationship between the urinary concentration of 6-sulphatoxymelatonin, a biomarker of melatonin concentration, and the incidence of breast cancer [100]; levels of 6-sulphatoxymelatonin decreased with increasing number of nights worked in the 2 weeks prior to urine collection [101]. However, another cohort study in the general population did not find such a relationship [102]. In classifying shift work that involves circadian disruption as probably carcinogenic to humans, IARC concluded that there was sufficient evidence in experimental animals for the carcinogenicity of light during the daily dark period (biological night) [49].
Clearly, more studies in humans are needed to allow a thorough understanding of the relationship between shift work and the incidence of breast cancer. A working group convened by the IARC identified several major domains of non-day shift schedules that needed to be captured in a consistent manner to increase the validity of future studies on shift work and cancer [72], and although a few studies already addressed these issues, more evidence needs to be gathered [90].
Occupational Circumstances with Insufficient Evidence for Carcinogenicity to the Human Breast
A few additional agents have been found to be associated with an increased breast cancer risk in women, but the weight of evidence in these studies was not deemed sufficient to support their classification as carcinogenic to the human breast (see Table 24.5).
Ionizing Radiation
Although all forms of ionizing radiation are accepted carcinogens, as they cause direct DNA mutagenesis (in particular double-stranded DNA breaks) and genomic instability [18], studies of occupational exposures to X-radiation or γ-radiation, neutron radiation, or radionuclides emitting α- or β-particles have been largely negative. Limitations of these studies were that the studied cohorts were small and their exposures were much lower than those of atomic bomb survivors or women who underwent radiation therapy.
Occupational exposures occur when either handling radioactive materials or being exposed to natural sources of radiation at work. Aircraft personnel are exposed to cosmic rays that are natural sources of γ-radiation and neutrons, and underground miners to natural radionuclides emitting essentially α-particles. Workers handling radioactive materials or machinery can be exposed to several types of radiation: for example, healthcare workers are exposed in larger numbers to X-radiation, but some may be exposed to radionuclides emitting α- or β-particles; industrial radiographers are exposed to X-radiation; and nuclear energy or nuclear weapon workers are essentially exposed to γ-radiation and α- or β-particles [18]. In 2008, the United Nations Scientific Committee on Exposure to Atomic Radiation estimated that about 22.8 million workers were exposed to ionizing radiation, with 13 million exposed to natural sources and 9.8 million to artificial sources; medical workers are considered to constitute about two-thirds of exposed workers [152]. The doses were relatively low: the annual occupational effective doses have been diminishing and were estimated to vary between 0.1 and 1.0 mSv per year in 2000–2002 for exposures to artificial sources, compared to 2.9 mSv per year for exposure to radon gas [152].
The IARC Working Group that assessed the available evidence of a relationship between breast cancer and occupational exposure to ionizing radiation (X-radiation and γ-radiation) among radiologists and radiology technicians remarked that increased risks appeared to be restricted to women exposed before the 1940s and to women who had been working for more than 30 years as certified radiology technicians [18]. A study of Chinese medical X-ray workers reported increased risks that were more elevated among women who began working before 1970 and before 30 years of age and those with more than 25 years of employment [103]. A small case-control study nested in the same Chinese cohort showed a non-significant exposure–response relation with increasing cumulative dose [153]. This pattern of higher risks among women born before 1940 and 1930 was also confirmed in a study of radiology technicians in the United States [104] and in a follow-up of that same cohort until 2008 [154]. Indeed, most recent cohort studies have not shown evidence of increased risks at current exposure levels [24, 105, 155]. A recent review of epidemiological studies of medical radiation workers concluded that information on average annual exposure to occupational radiation, time trends in radiation exposure, and organ-specific doses was insufficient in most of the available studies to assess the lifetime cancer risk of these workers. The authors stressed the importance of conducting large-scale studies where individual cumulative occupational radiation dose estimates are used to assess dose–response relationships [156].
The available cohort studies of uranium production and of nuclear energy workers have very small numbers of female workers, and consequently very low power to detect increased risks of breast cancer. Cohort studies of workers at a few uranium mines or production facilities in the United States (primarily α-radiation from dusts) did not show any increased incidence or mortality rates of breast cancer among exposed workers, and a small increase was observed among nonexposed workers [106, 157]. A cohort study of French nuclear energy production workers reported a small increased risk of death due to breast cancer (standardized mortality ratio 1.14, 90% CI 0.94–1.37) [107], whereas a study of French uranium fuel cycle workers showed a higher but still non-significant increased risk (standardized mortality ratio 1.53, 95% CI 0.94–2.37) [158]. One case-control study showed a large increased risk (OR 5.3, 95% CI 2.4–14.1) associated with exposure to ionizing radiation, but used rather crude exposure assessment methods (expert assessment based on occupational history) [108]. Another case-control study estimated occupational exposure to ionizing radiation using automatic assignments to occupational histories; it showed an increased risk of human epidermal growth factor receptor 2-positive (HER2+) breast cancer with occupational exposure in premenopausal women (OR = 2.57; 95% confidence interval, 1.09–6.03) [159]. An analysis of the Canadian National Dose Registry did not show an excess risk of breast cancer in women with occupational exposure to ionizing radiation [160]. As exposure decreases over the years, risks are presumably being reduced and very large studies will be needed to detect excess risks.
Polychlorinated Biphenyls (PCBs)
PCBs are a group of 209 aromatic hydrocarbons that were widely used because of several interesting properties (non-flammability, chemical stability, high boiling point, and high dielectric constant). Although their production and use was banned worldwide (dates vary from the 1970s in the United States to 2006 in Korea), they can still be found in numerous products manufactured before the ban. Workers are therefore mainly exposed during abatement in construction, in waste incineration, and recycling of electronic equipment and fluorescent lights [47]. PCBs were classified as carcinogenic to humans, with sufficient evidence for malignant melanoma, and limited evidence for breast cancer [47].
The available evidence for breast cancer comes from case-control studies based on levels of PCBs measured in serum and adipose tissues of women, without certainty on the source of exposure [47]. The occupational data comes mainly from mortality studies of capacitor manufacturing cohorts with small numbers of female workers; these mortality studies were negative [114, 161], and only one suggested a relatively small increased risk of breast cancer incidence following occupational exposure to PCBs [113]. Thus, the extent to which occupational exposures to PCBs can be linked to increased incidence of breast cancer is still debated.
Dieldrin
Dieldrin (and aldrin, which is metabolized into dieldrin) is an organochlorine pesticide that has been banned since the 1970s in several countries because of environmental concerns on its environmental persistence [162]. Dieldrin is still measurable in the air, soil, ground water, and food in several developing [163, 164] and developed countries [165, 166]. Dieldrin was classified as probably carcinogenic to humans, with limited evidence for breast cancer [162].
As for PCBs, most of the evidence for breast cancer comes from studies based on serum levels of dieldrin. A prospective Danish study found a significant dose–response relationship between the risk of breast cancer and increasing serum dieldrin levels [167, 168], whereas a similar study in Norway was negative [169]. Positive associations with breast cancer were also reported in spouses of men who had used dieldrin in the US Agricultural Health Study, regardless of their own direct exposure to the pesticide [115, 116]. Hence, there appears to be an association between dieldrin burden and the incidence of breast cancer, but the importance of the contribution of occupational exposure to the increased risk will probably not be elucidated given the ban of organochlorine pesticides.
Occupational Exposure to Hormones, Antineoplastic Drugs, or Other Pharmaceuticals
So far, a few pharmaceutical drugs have been classified as carcinogenic or probably carcinogenic to the female breast of treated patients. Among these, diethylstilbestrol used during pregnancy, oral contraceptives or hormone replacement therapy containing estrogens only or estrogen-progestogen combinations [13] and digoxin [170] have been classified as carcinogenic (Group 1 agents) by the IARC. However, occupational exposures to these pharmaceuticals were not addressed in the corresponding issues of the IARC Monographs, other than to report on chromosomal aberrations in healthcare personnel handling antineoplastic drugs [13].
Several studies among pharmaceutical and healthcare workers reported evidence of elevated levels of urinary metabolites of antineoplastic drugs [171], or of effects linked to exposure to steroids (e.g., gynecomastia and loss of libido in men and menstrual problems in women) [172]. However, only a few epidemiological studies reported, more than 20 years ago, on the risk of cancer among pharmaceutical workers. Elevated risks of breast cancer in the order of 1.5–2.9 were reported in a Danish record-linkage study [136] and in two of four cohort studies of pharmaceutical workers [173, 174]. Another cohort study reported a small increase in incidence among women in the highest exposure groups [137], whereas in the fourth cohort study, only mortality was assessed and there were very few breast cancer deaths to draw conclusions [138]. Not enough data are available to draw conclusions about whether the fabrication or handling of pharmaceutical drugs is associated with an increased risk of breast cancer.
Other Occupational Exposures
The available evidence for other occupations or occupational exposures comes from studies that have varying levels of precision. Linkage studies combining records or registries have usually relied on occupation and/or industry titles, whereas other designs such as case-control or cohort studies have complemented job titles and industry with information on specific exposures gathered by questionnaires or derived from job-exposure matrices. During the last 15 years, few studies have been conducted on the role of other occupational exposures in female breast cancer.
Organic Solvents and Aromatic Hydrocarbons
There is some evidence of increased breast cancer risk associated with exposures to several categories of organic solvents, including halogenated solvents [117,118,119] and solvents that metabolize into reactive oxygen species [120]. Industries and occupations that entail exposure to organic solvents have also been associated with increased breast cancer risk [121, 175]: laundry and dry cleaning occupations; working in the aircraft and automotive industries, including service attendants at gasoline stations [122]; electronic workers and those in semiconductor plants [118, 123, 124]; and printing machine operators and tenders [123]. However , in some studies the risks were very low [124, 125] or even nonexistent, such as for styrene [126]. Etiological factors for breast cancer appear to differ according to the hormonal receptor status of the tumor. For example, exposure to solvents appears to increase the risk of breast tumors with certain hormonal receptor status, such as estrogen receptor-positive tumors [120, 175] and some progesterone-negative tumors [119, 120]; younger age at first exposure appears to increase the risk [117, 118, 120, 175].
Aromatic hydrocarbons are a large family of molecules containing at least one benzene ring (i.e., a six-carbon structure with alternating double and single bonds between carbon atoms). Some of these are also considered organic solvents, and the simplest of these chemicals is benzene; aromatic hydrocarbons with one benzene ring are called monocyclic aromatic hydrocarbons (MAHs), whereas those with two or more fused benzene rings are referred to as polycyclic aromatic hydrocarbons (PAHs) [176]. PAHs are derived from incomplete combustion of organic material, and their concentrations are influenced particularly by industrial and traffic-related sources [48, 176]. Some PAHs are carcinogenic in humans, while a few others are classified as probably or possibly carcinogenic to humans.
Exposure to benzene [128], to MAHs as a group [120], and to PAHs [129] has been associated with an increased incidence of about 30%, but not consistently [177]. The increased risk has been observed in both premenopausal [128] and postmenopausal women [120]. The effects of exposure to PAHs appear to be influenced by genetic susceptibility [178]. Aromatic amines, a subgroup of aromatic hydrocarbons often used as pigments, have also been found to be associated with an increased risk of breast cancer, with a clear exposure–response relationship [179], and with risk patterns that may differ according to the hormonal receptor status of the tumor [180]. Finally, a small risk has also been reported for exposure to soluble metalworking fluids [181].
Extremely-Low-Frequency Electric and Magnetic Fields
In 2000, a review of the literature concluded that occupational exposure to extremely-low-frequency electric and magnetic fields (ELF-EMFs) could possibly be associated with female breast cancer [182]. However, in its 2002 monograph on nonionizing radiation, the IARC mentioned such a possible increased risk of breast cancer among men, without referring to female breast cancer. It was also pointed out that the available studies on women from the 1980s and early 1990s had presented methodological limitations, including lack of appropriate exposure measurements, and a possible publication bias toward those studies showing positive associations [183]. Moreover, Goodman and colleagues studied the effect of uncontrolled potential confounding factors in early studies of EMF exposure and concluded that they could account for an OR of about 1.2–1.3 [184].
More recent studies, including meta-analyses, have not found that exposure to EMFs increases the risk of female breast cancer [131, 185,186,187]. Specifically, a large population-based case-control study showed a slight increase in risk [132], whereas another case-control study showed a fourfold increased risk among telephone and telegraph operators [133]. A few additional studies suggested a moderately increased risk for postmenopausal breast cancer in certain subgroups of women, such as those exposed before age 36 years and whose tumor was progesterone-positive [134], and premenopausal women with estrogen receptor-positive breast cancer were associated with a long duration of high occupational exposures [135].
Other Pesticides and Other Organochlorines
Results from most of the recent studies show either none or only a very small increased risk of breast cancer after exposure to pesticides [188] or other organochlorines [189]. However, one cohort study of chemical workers exposed to dioxins showed an increase of breast cancer mortality (standardized mortality ratio (SMR) = 1.86) based on 19 deaths, but no clear exposure–response pattern [190]. In a few recent papers, increased risks were linked to certain polymorphisms, notably of cytochrome P-450 1A1 [191] and GSTM1 [192]: it is possible that small increased risks of breast cancer do exist, but only in the presence of certain polymorphisms.
Specific Job Titles
The first published mention of an “occupational” increased risk of breast cancer occurred more than 300 years ago by Bernardino Ramazzini, who reported on increased occurrence of breast cancer among nuns, which he attributed to celibacy, sensing a relationship with nulliparity [193]. Several clerical and professional occupations, such as those of administrators, teachers, librarians, journalists, inspectors, and others, have repeatedly been associated with an increased risk of incidence or mortality in different settings, often in studies based on routinely collected data [129, 130, 133, 150, 194,195,196,197,198]. The increased risk presented by these professional occupations has been ascribed by most authors [129, 130, 150, 196, 197, 199] (but not all [198]) to peculiar reproductive and other lifestyle factors and residual confounding associated with indicators of higher socioeconomic status that would be more frequent among women occupying these professions: high education level; having less children, at a later age; higher use of hormone replacement therapy; and higher alcohol consumption.
Increased risks have also been reported for farming occupations [133, 142], textile and clothing workers [108, 130, 200], leather and fur processors and glass-manufacturing workers [133], nurses [61], dentists [201], electricity power plant workers [202], semiconductor and computer manufacturing industries [125, 149], metalworking and automotive plastics manufacturing [203], rubber industry workers [179, 200], and scientists and laboratory workers [141, 150]. However, similar occupations have also been associated with absence of risk in other studies, for example, the occupation of farm worker [130, 204,205,206], garment worker [143], glass manufacturer [129], dentist [201], and cosmetologist and manicurist [151].
Air transport crews, particularly flight attendants, showed increased risks of female breast cancer in several studies in the Nordic countries and in the United States [207]. After adjusting for possible confounding by reproductive factors, a few studies still showed an increased risk [144, 145] although there were a few negative studies [146,147,148, 208, 209].
In summary, several high-quality studies have been conducted, but our understanding of how occupational and environmental agents affect female breast cancer risk is still limited partly because of inconsistencies and partly because only a handful of potentially hazardous agents have been investigated. In many studies on specific industries or occupations, other lifestyle factors known to be associated with breast cancer (such as alcohol consumption, lower parity, and late age at first full-term pregnancy) were often not taken into account, so confounding could not be ruled out. Subtleties of the mechanistic relationships are also difficult to capture in epidemiological analyses, due to difficulties in past exposure assessment, not knowing the ages at which women may be highly susceptible, and because effects may be restricted to a subset of women with specific genotypes.
Other Inconclusive Environmental Exposures
Cadmium and other heavy metals that have estrogenic activity in animal studies have been postulated to be associated with increased risks [210], but little human data are available and the association with human breast cancer remains unclear [211].
Since the improvement and accessibility of traffic-related air pollution exposure assessments, a handful of studies on traffic-related air pollution exposure and breast cancer have been conducted. In a case-control study based in New York State, an association was found with increased volumes of vehicular traffic [212] and higher concentrations of total suspended particulates were associated positively with exposures to benzo[a]pyrene [213, 214]. In the Nurses’ Health Study II, no associations were found for incident breast cancer and fine particulates, but increased rates were found among premenopausal and postmenopausal women living within 50 m of major roads [215]. In the Sister Cohort [216], increased risks for nitrogen dioxide (NO2) exposure measured by fixed-site monitors were also found among cases with positive estrogen receptor and positive progesterone receptor status (hazard rate: 1.10; 95% CI: 1.02–1.19). A hospital-based case-control study by Crouse and colleagues [217] reported increased risks of postmenopausal breast cancer with exposure to traffic-related air pollution in Montreal, using ground-level concentrations of nitrogen dioxide, a reliable marker of traffic-related air pollution. A subsequent population-based case-control study of postmenopausal breast cancer from 2008 to 2011 was conducted by Goldberg and colleagues [218] in the same city. They found an increased breast cancer risk per increase in the interquartile range (IQR = 5.8 ppb) of NO2: OR: 1.10; 95% CI: 1.02–1.19. The study was also the first to examine associations of breast cancer with ultrafine particles (<0.1 μm in aerodynamic diameter); however, there was little evidence of association in any of the models or sub-analyses and little variability in the ORs. In another population-based case-control study conducted in eight provinces of Canada from 1975 to 1994, positive associations between incident premenopausal breast cancer and ground-level concentrations of NO2 were found: for a 10 part per billion (ppb) the ORs varied between 1.26 and 1.32 and the 95% confidence intervals excluded the null. Lower ORs were found for postmenopausal breast cancer, in the order of 1.10 [219].
Air pollution is a complex chemical and physical mixture, and many of the pollutants are also found in the workplace. Indeed, a few studies have shown associations between the incidence of breast cancer and occupational exposure to chemicals that are present in vehicular exhaust and thus in urban air pollution, such as benzene, carbon monoxide, and PAHs [119, 120, 127]. Should traffic-related air pollution prove to be a risk factor, a very large number of cases may be attributed to it, as exposure is ubiquitous in both working and nonworking populations.
Interaction Between Genetic Susceptibility and Various Exposures
The study of joint effects of genetic and environmental factors is crucial in understanding the etiology of breast cancer because it allows the identification of subgroups of women with specific genotypes who may be at higher risk after exposure to xenobiotics or whose risk may be reduced by other exposures [220]. These studies provide insights into mechanisms and can help to determine possible enzymes or proteins that can act on potential carcinogens [220]. For example, if null alleles are present in detoxification reactions (e.g., no enzyme synthesized), carcinogens or carcinogenic metabolites, especially lipophilic ones, may concentrate in adipose breast tissue. A major issue in such studies is having sufficient statistical power, and only studies with thousands of subjects can produce reliable results, and many of the studies reported below may not have been large enough.
A few gene–environment studies have reported that certain single-nucleotide polymorphisms (SNPs) involved in the biotransformation of xenobiotics are associated with increased breast cancer risk. Numerous polymorphisms of P-450 cytochromes have been identified, and further study of gene–environment interactions has been recommended [221]. In a German study [222], urinary concentrations of metabolites of PAHs were associated with certain polymorphisms of CYP1A1 and GSTP1. Elevated relative risks of breast cancer were found for high levels of plasma PCBs and CYP1A1 variants in case-control studies [223, 224] and in the Nurses’ Health Study [225], but in another case-control study no associations between occupation and CYP1A1∗2 polymorphisms [226] were found. Results between the risk of breast cancer and exposure to smoking or second hand tobacco smoke are inconsistent in relation to slow and rapid NAT2 acetylators [227,228,229], and with exposures to aromatic and heterocyclic amines [180]. Elevated risks of breast cancer were suggested for current alcohol consumption with certain glutathione S-transferase genotypes (null GSTM1, GSTT1, and GSTM3) [230,231,232], and there was an inverse association between breast cancer risk and frequency of alcohol consumption with alcohol dehydrogenase II polymorphism [233]. The Breast Cancer Association Consortium recently published an analysis of the interaction between 70 single-nucleotide polymorphisms (identified by genetic fine-scale mapping of susceptibility loci) and 11 breast cancer risk factors: they notably found interactions between CFLAR-rs7558475 and current smoking, and between 5q14-rs7707921 and alcohol consumption for estrogen-receptor-negative tumors [234].
It has also been determined that carriers of two high-risk alleles, BRCA1 and BRCA2, show increased sensitivity to the effect of clastogens as measured by micronucleus formation [235]. Polymorphisms of p53, a protein involved in the regulation of the cell cycle and apoptosis, were associated with increased risks in association with exposures to ionizing radiation in the Carolina Breast Cancer Study [236].
In summary, several studies have shown that interactions between certain genetic variants and exposure to xenobiotics can affect the risk of breast cancer, but the findings still need to be replicated before any firm etiologic conclusion can be drawn.
Proportion of Female Breast Cancer Attributable to Occupation
As of 2017, four groups of researchers had published estimates of the burden of breast cancer attributable to occupational exposures now or in the future. The first study included ionizing radiation and exposure to hair dyes among hairdressers and concluded that 1.7% of breast cancer in Finland could be attributed to occupational exposures [237]. The second study, considering shift work and flight personnel, estimated that 4.6% of female breast cancers in Great Britain could be attributed to occupational exposures [238]. The third study calculated that 5.7% of breast cancers in the United States could be attributed to shiftwork [239]. Finally, the last study predicted that 0.7% of breast cancers diagnosed among women at work in 2012, until they are 100 years of age, would be caused by exposure, as of 2012, to ionizing radiation, ethylene oxide, and shift work [240] (see Table 24.6).
Male Breast Cancer
Descriptive Epidemiology
Male breast cancer is a very rare disease, with incidence rates varying from 0.1 to 2 per 100,000 men worldwide [241]. Rates are higher in North America and Europe (estimated at 0.47 per 100,000 [242]) and extremely low in Asian populations. Indeed, female breast cancer incidence is 100 times higher than male breast cancer incidence, which represents less than 1% of all breast cancers worldwide [241]. Studies on the time trends of male breast cancer indicate that its incidence is increasing in North America, the United Kingdom, Singapore, and possibly some African countries, mimicking time trends of female breast cancer although on a much smaller scale. Conversely, in the Nordic countries and Switzerland, incidence has been stable over the last 40 years [243,244,245].
General Epidemiology and Lifestyle-Related Risk Factors
The etiology of male breast cancer is poorly understood. This may be due to the rarity of the disease and, consequently, the scarcity of published studies. Genetic, hormonal, and environmental risk factors have been reported to be associated with male breast cancer risk. Family history of breast cancer has been associated with an increased risk of male breast cancer [27]. In particular, genetic susceptibilities related to male breast cancer include mutations in BRCA1, BRCA2, and possibly other genes (CYP17, AR gene, CHEK2) [246]. Klinefelter’s syndrome and a few other rare disorders have also been associated with increased risk. Similarly, associations with education, religion, marital status, clinical disorders related to hormonal imbalance (e.g., infertility, testicular injury, gynecomastia), and estrogen intake are controversial. Hormonal imbalance appears to lend to an increased risk [247].
Among the lifestyle exposures studied, alcohol consumption and related liver cirrhosis, heavy tobacco smoking, and obesity were associated with increased male breast cancer risk in a few studies, but results were equivocal. There are an insufficient number of studies to allow any conclusions about the effect of exposure to ionizing radiation or electromagnetic fields on male breast cancer [247,248,249,250,251]. So far, the IARC has not identified any carcinogens specifically for male breast cancer.
Occupational Exposures
Some evidence of carcinogenicity to the male human breast has been gathered for Group 1 agents outside the occupational setting, e.g., alcoholic beverages [249] and X-radiation and γ-radiation [109, 252]. Some evidence of a relationship with occupational ionizing radiation exposure has also been reported [110], and a recent analysis of the Japanese Atomic Bomb Survivors data reported higher radiation-associated relative risk for male breast cancer compared to the risk in women [253].
Inconclusive Occupational Exposures
A few occupational exposures have been associated, albeit inconclusively, with male breast cancer [246, 247, 254].
Extremely-Low-Frequency Electric and Magnetic Fields
In its 2002 monograph , the IARC Working Group on nonionizing radiation mentioned a possible increased risk of male breast cancer in association with ELF-EMFs. The committee also pointed out that the available studies from the 1980s and early 1990s presented methodological limitations, lack of appropriate exposure measurements, and a possible positive publication bias [183]. Since then very few studies and one meta-analysis have been published regarding male breast cancer risk. A modest increased risk of male breast cancer (OR of 1.31, 95% CI 0.94–1.81) has been reported in men exposed to ELF-EMFs above 0.12 microteslas (exposure attributed using a job-exposure matrix); those exposed intermittently showed indications of an exposure–response trend, which led the authors to conclude that variations in exposure levels within work days could be associated with an increased risk [255]. In a meta-analysis of 18 cohort and case-control studies, a pooled risk estimate of male breast cancer of 1.32 (95% CI 1.10–1.59) was estimated with any occupational exposure to EMF from seven studies that used job title or a job-exposure matrix to assess exposure [256]. In conclusion, the available evidence does not allow to draw firm conclusions on the effect of exposure to ELF-EMFs on male breast cancer risk.
Polycyclic Aromatic Hydrocarbons and PCBs
The few epidemiological studies investigating the relationship between exposure to PAHs and male breast cancer did not show consistent findings. In a record-linkage study, Hansen [257] reported a significantly increased risk among workers potentially exposed to combustion products (as a proxy for PAHs) when compared with other workers; the risk was particularly elevated for exposures starting before age 40 years [257]. However, in an Italian case-control study, no association was found between male breast cancer and occupational exposure to PAHs [258]. Two recent studies of capacitor workers showed non-statistically significant increases in mortality and in incidence of male breast cancer based on very little numbers ([259], based on two deaths; [161], based on six cases).
Heat
A few reviews mentioned that occupational exposure to high temperatures has been associated with increased risk of breast cancer in men, possibly because of testicular dysfunction resulting from high temperatures [246, 247]. However, these reviews refer to a small number of studies with a number of methodological limitations. Three small case-control studies (52, 91, and 71 cases) reported an increased risk for men “with occupations that involved heat exposure” [260,261,262], whereas a larger one reported that working in blast furnaces, steel works, and rolling and finishing mills (occupations with elevated heat exposures) conveyed a threefold increased risk of male breast cancer [258]. Nevertheless, several other carcinogens are also found in these workplaces and their potential confounding effects cannot be excluded.
Various Occupations
In 1842, Domenico Antonio Rigoni-Stern reported an increased occurrence of breast cancer among male priests, but his findings have not been confirmed in more recent studies [248, 263,264,265]. A cohort study of men exposed to ethylene oxide (a carcinogen linked to breast cancer in women) did not report the occurrence of breast cancer in the studied workers [266]. A large study carried out in the Nordic countries reported higher than expected standardized incidence rates among journalists, cooks, stewards, printers, artistic workers, and building caretakers [129]; the authors underscore a common characteristic of these occupations—they usually include shift work, which has been associated with increased breast cancer risk in women [49]. A significantly increased risk of dying from breast cancer has been reported in policemen [267] and in professional firefighters [268, 269], but the incidence of breast cancer was not increased in the same cohort [270]. More recent studies of firefighters showed non-significant increases of incidence [269, 271] or of both mortality and incidence [271]. A European case-control study found a twofold increased risk, possibly due to petroleum and other organic solvents, especially among motor vehicle mechanics and painters. The risk was also increased for elevated exposure to alkylphenolic compounds, which are known endocrine-disrupting chemicals (OR 3.8, 95% CI 1.5–9.5) [272]. One study reported a relationship between carrier status for BRCA1/2 mutations and the occupation of truck driver in male breast cancer risk [273].
Conclusion
In conclusion, a handful of occupational exposures have been linked, with reasonable evidence, to an increased risk of breast cancer in women, but none have yet been linked to male breast cancer, although similarities between male and female breast cancers [274] suggest potential common causal factors. As the most common cancer among women, breast cancer represents an important global burden. There are no certainties regarding the importance of occupational or environmental exposures in the etiology and development of breast cancer, but the fact that only about 30% of the risk is explained by known risk factors [272] means that continuous research on the relationship between occupational exposures and breast cancer is warranted.
Breast cancer risk is influenced by a number of hormonal factors and may thus be influenced by endocrine-disrupting agents. These exposures may be mediated by environmental determinants, such as lifestyle (hormone therapy, diet, alcohol consumption, smoking), work schedule (e.g., shift work), and various medical conditions. As the mammary gland passes through certain critical periods during development, particularly in women, adverse effects may necessitate exposure to carcinogens during the short window of time when the structures of the gland are sensitive. These toxicants could lead to an increase in the incidence of mammary tumors if they alter circulating or tissue-localized hormone levels. This could happen through mechanisms such as hormonal disruption, mutations in critical genes caused by alkylating carcinogens during key stages of development, or influences on hormone transport and receptor expression patterns.
While there are many critical periods during mammary gland development and a large array of potential toxicants which may be able to act as cancer-causing agents under some conditions in experimental models, there are not many that have been shown to do so in humans. However, it is ultimately the observations in humans that will dictate if what is possible from a theoretical point of view can happen in real-life situations. The issues involved, such as the possible interactions between potential risk factors, including critical exposures before complete maturation of the breast gland, and the great diversity of breast cancer itself, are very complex and challenging to study in humans.
The absence of specific molecular markers and genetic susceptibility tests hampers early identification of women and men who would be particularly susceptible to occupation-related breast cancer, but does not preclude preventive activities that are well known to the occupational hygiene field: anticipation of potential carcinogens, followed by their recognition, evaluation, communication, and control (elimination, substitution, and reduction of exposure) in the workplace.
References
Bray F, Ferlay J, Soerjomataram I, Siegel RL, Torre LA, Jemal A. Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries. CA Cancer J Clin. 2018;68:394–424.
Jemal A, Ward E, Thun MJ. Recent trends in breast cancer incidence rates by age and tumor characteristics among U.S. women. Breast Cancer Res. 2007;9:R28.
Ravdin PM, Cronin KA, Howlader N, et al. The decrease in breast-cancer incidence in 2003 in the United States. N Engl J Med. 2007;356:1670–4.
Althuis MD, Dozier JM, Anderson WF, Devesa SS, Brinton LA. Global trends in breast cancer incidence and mortality 1973–1997. Int J Epidemiol. 2005;34:405–12.
Kelsey JL, Bernstein L. Epidemiology and prevention of breast cancer. Annu Rev Public Health. 1996;17:47–67.
Harris JR, Lippman ME, Veronesi U, Willett W. Breast cancer (1). N Engl J Med. 1992;327:319–28.
Byrne C, Harris A. Cancer rates and risks. 4th ed. Bethesda: US Department of Health and Human Services, National Institutes of Health; 1996.
Gail MH, Brinton LA, Byar DP, Corle DK, Green SB, Schairer C, Mulvihill JJ. Projecting individualized probabilities of developing breast cancer for white females who are being examined annually. J Natl Cancer Inst. 1989;81:1879–86.
Rockhill B, Weinberg CR, Newman B. Population attributable fraction estimation for established breast cancer risk factors: considering the issues of high prevalence and unmodifiability. Am J Epidemiol. 1998;147:826–33.
Madigan MP, Ziegler RG, Benichou J, Byrne C, Hoover RN. Proportion of breast cancer cases in the United States explained by well-established risk factors. J Natl Cancer Inst. 1995;87:1681–5.
Bruzzi P, Green SB, Byar DP, Brinton LA, Schairer C. Estimating the population attributable risk for multiple risk factors using case-control data. Am J Epidemiol. 1985;122:904–14.
Collaborative Group on Hormonal Factors in Breast Cancer. Breast cancer and breastfeeding: collaborative reanalysis of individual data from 47 epidemiological studies in 30 countries, including 50302 women with breast cancer and 96973 women without the disease. Lancet. 2002;360:187–95.
IARC. Monographs on the evaluation on carcinogenic risks to humans. A review of human carcinogens. Part A: pharmaceuticals, vol. 100. Lyon: International Agency for Research on Cancer; 2011.
World Cancer Research Fund, American Institute for Cancer Research. Food, nutrition, physical activity, and the prevention of cancer: a global perspective. Washington, DC: AICR; 2007.
Ewertz M. Hormone therapy in the menopause and breast cancer risk—a review. Maturitas. 1996;23:241–6.
IARC. IARC handbooks of cancer prevention, weight control and physical activity, vol. 6. Lyon: International Agency for Research on Cancer; 2002.
IARC. IARC handbooks of cancer prevention, fruit and vegetables, vol. 8. Lyon: International Agency for Research on Cancer; 2003.
IARC. Monographs on the evaluation on carcinogenic risks to humans. A review of human carcinogens. Part D: radiation, vol. 100. Lyon: International Agency for Research on Cancer; 2012.
Hankinson S, Hunter D. Breast cancer. In: Hunter H, Trichopoulos D, Adami HO, editors. Textbook of cancer epidemiology. Oxford: Oxford University Press; 2002.
Ekenga CC, Parks CG, Sandler DP. A prospective study of occupational physical activity and breast cancer risk. Cancer Causes Control. 2015;26:1779–89.
Johnsson A, Broberg P, Johnsson A, Tornberg AB, Olsson H. Occupational sedentariness and breast cancer risk. Acta Oncol. 2017;56:75–80.
IARC. Monographs on the evaluation on carcinogenic risks to humans. A review of human carcinogens. Part E: personal habits and indoor combustions, vol. 100. Lyon: International Agency for Research on Cancer; 2012.
Boice JD Jr, Monson RR. Breast cancer in women after repeated fluoroscopic examinations of the chest. J Natl Cancer Inst. 1977;59:823–32.
Ahn YS, Park RM, Koh DH. Cancer admission and mortality in workers exposed to ionizing radiation in Korea. J Occup Environ Med. 2008;50:791–803.
Antoniou AC, Easton DF. Models of genetic susceptibility to breast cancer. Oncogene. 2006;25:5898–905.
Goldgar DE, Easton DF, Cannon-Albright LA, Skolnick MH. Systematic population-based assessment of cancer risk in first-degree relatives of cancer probands. J Natl Cancer Inst. 1994;86:1600–8.
Slattery ML, Kerber RA. A comprehensive evaluation of family history and breast cancer risk. The Utah population database. JAMA. 1993;270:1563–8.
Mavaddat N, Antoniou AC, Easton DF, Garcia-Closas M. Genetic susceptibility to breast cancer. Mol Oncol. 2010;4:174–91.
Amundadottir LT, Thorvaldsson S, Gudbjartsson DF, et al. Cancer as a complex phenotype: pattern of cancer distribution within and beyond the nuclear family. PLoS Med. 2004;1:e65.
Kerber RA, O’Brien E. A cohort study of cancer risk in relation to family histories of cancer in the Utah population database. Cancer. 2005;103:1906–15.
Stratton MR, Rahman N. The emerging landscape of breast cancer susceptibility. Nat Genet. 2008;40:17–22.
Pharoah PD, Antoniou A, Bobrow M, Zimmern RL, Easton DF, Ponder BA. Polygenic susceptibility to breast cancer and implications for prevention. Nat Genet. 2002;31:33–6.
Rahman N, Seal S, Thompson D, et al. PALB2, which encodes a BRCA2-interacting protein, is a breast cancer susceptibility gene. Nat Genet. 2007;39:165–7.
Easton DF, Pooley KA, Dunning AM, et al. Genome-wide association study identifies novel breast cancer susceptibility loci. Nature. 2007;447:1087–93.
Hunter DJ, Kraft P, Jacobs KB, et al. A genome-wide association study identifies alleles in FGFR2 associated with risk of sporadic postmenopausal breast cancer. Nat Genet. 2007;39:870–4.
Ahmed S, Thomas G, Ghoussaini M, et al. Newly discovered breast cancer susceptibility loci on 3p24 and 17q23.2. Nat Genet. 2009;41:585–90.
Stacey SN, Manolescu A, Sulem P, et al. Common variants on chromosome 5p12 confer susceptibility to estrogen receptor-positive breast cancer. Nat Genet. 2008;40:703–6.
Thomas G, Jacobs KB, Kraft P, et al. A multistage genome-wide association study in breast cancer identifies two new risk alleles at 1p11.2 and 14q24.1 (RAD51L1). Nat Genet. 2009;41:579–84.
Turnbull C, Ahmed S, Morrison J, et al. Genome-wide association study identifies five new breast cancer susceptibility loci. Nat Genet. 2010;42:504–7.
Zheng W, Long J, Gao YT, et al. Genome-wide association study identifies a new breast cancer susceptibility locus at 6q25.1. Nat Genet. 2009;41:324–8.
Cox A, Dunning AM, Garcia-Closas M, et al. A common coding variant in CASP8 is associated with breast cancer risk. Nat Genet. 2007;39:352–8.
Milne RL, Benitez J, Nevanlinna H, et al. Risk of estrogen receptor-positive and -negative breast cancer and single-nucleotide polymorphism 2q35-rs13387042. J Natl Cancer Inst. 2009;101:1012–8.
Antoniou AC, Wang X, Fredericksen ZS, et al. A locus on 19p13 modifies risk of breast cancer in BRCA1 mutation carriers and is associated with hormone receptor-negative breast cancer in the general population. Nat Genet. 2010;42:885–92.
Wacholder S, Hartge P, Prentice R, et al. Performance of common genetic variants in breast-cancer risk models. N Engl J Med. 2010;362:986–93.
IARC. Agents classified by the IARC monographs, vol. 1–120. Lyon: International Agency for Research on Cancer. http://monographs.iarc.fr/ENG/Classification/ClassificationsGroupOrder.pdf. Last update 27 Oct 2017.
IARC. Website of the IARC monographs on the evaluation of carcinogenic risks to humans. http://monographs.iarc.fr/. Accessed 27 Oct 2017.
IARC. Monographs on the evaluation on carcinogenic risks to humans. A review of human carcinogens. Polychlorinated and polybrominated biphenyls, vol. 107. Lyon: International Agency for Research on Cancer; 2015.
IARC. Monographs on the evaluation on carcinogenic risks to humans. A review of human carcinogens. Part F: chemical agents and related occupations, vol. 100. Lyon: International Agency for Research on Cancer; 2012.
IARC. Monographs on the evaluation on carcinogenic risks to humans. Painting, firefighting and shiftwork, vol. 98. Lyon: International Agency for Research on Cancer; 2010.
Hagmar L, Mikoczy Z, Welinder H. Cancer incidence in Swedish sterilant workers exposed to ethylene oxide. Occup Environ Med. 1995;52:154–6.
Norman SA, Berlin JA, Soper KA, Middendorf BF, Stolley PD. Cancer incidence in a group of workers potentially exposed to ethylene oxide. Int J Epidemiol. 1995;24:276–84.
Steenland K, Whelan E, Deddens J, Stayner L, Ward E. Ethylene oxide and breast cancer incidence in a cohort study of 7576 women (United States). Cancer Causes Control. 2003;14:531–9.
Coggon D, Harris EC, Poole J, Palmer KT. Mortality of workers exposed to ethylene oxide: extended follow up of a British cohort. Occup Environ Med. 2004;61:358–62.
Mikoczy Z, Tinnerberg H, Bjork J, Albin M. Cancer incidence and mortality in Swedish sterilant workers exposed to ethylene oxide: updated cohort study findings 1972-2006. Int J Environ Res Public Health. 2011;8:2009–19.
Schernhammer ES, Laden F, Speizer FE, Willett WC, Hunter DJ, Kawachi I, Colditz GA. Rotating night shifts and risk of breast cancer in women participating in the nurses’ health study. J Natl Cancer Inst. 2001;93:1563–8.
Schernhammer ES, Kroenke CH, Laden F, Hankinson SE. Night work and risk of breast cancer. Epidemiology. 2006;17:108–11.
Schwartzbaum J, Ahlbom A, Feychting M. Cohort study of cancer risk among male and female shift workers. Scand J Work Environ Health. 2007;33:336–43.
Pronk A, Ji BT, Shu XO, et al. Night-shift work and breast cancer risk in a cohort of Chinese women. Am J Epidemiol. 2010;171:953–9.
Tynes T, Hannevik M, Andersen A, Vistnes AI, Haldorsen T. Incidence of breast cancer in Norwegian female radio and telegraph operators. Cancer Causes Control. 1996;7:197–204.
Hansen J. Increased breast cancer risk among women who work predominantly at night. Epidemiology. 2001;12:74–7.
Lie JA, Roessink J, Kjaerheim K. Breast cancer and night work among Norwegian nurses. Cancer Causes Control. 2006;17:39–44.
Davis S, Mirick DK, Stevens RG. Night shift work, light at night, and risk of breast cancer. J Natl Cancer Inst. 2001;93:1557–62.
O’Leary ES, Schoenfeld ER, Stevens RG, et al. Shift work, light at night, and breast cancer on Long Island, New York. Am J Epidemiol. 2006;164:358–66.
Pesch B, Harth V, Rabstein S, et al. Night work and breast cancer—results from the German GENICA study. Scand J Work Environ Health. 2010;36:134–41.
NTP. “Ethylene oxide”. Report on carcinogens. 14th ed. Research Triangle Park: US Department of Health and Human Services, Public Health Service, National Toxicology Program; 2016. http://ntp.niehs.nih.gov/go/roc14/. Last update 3 Nov 2016.
Occupational Safety and Health Commission. Regulatory review of the occupational safety and health administration’s ethylene oxide standard. Washington, DC: OSHA; 2005.
Kauppinen T, Toikkanen J, Pedersen D, et al. Occupational exposure to carcinogens in the European union. Occup Environ Med. 2000;57:10–8.
Grosswald B. The effects of shiftwork on family satisfaction. Families in society. J Contemp Soc Serv. 2004;85:413–23.
Costa G, Haus E, Stevens R. Shift work and cancer—considerations on rationale, mechanisms, and epidemiology. Scand J Work Environ Health. 2010;36:163–79.
Megdal SP, Kroenke CH, Laden F, Pukkala E, Schernhammer ES. Night work and breast cancer risk: a systematic review and meta-analysis. Eur J Cancer. 2005;41:2023–32.
Brainard GC, Sliney D, Hanifin JP, et al. Sensitivity of the human circadian system to short-wavelength (420-nm) light. J Biol Rhythm. 2008;23:379–86.
Stevens RG, Hansen J, Costa G, et al. Considerations of circadian impact for defining ‘shift work’ in cancer studies: IARC working group report. Occup Environ Med. 2011;68:154–62.
Parent-Thirion A, Fernandez Macias E, Huntly J, Vermeylen G. Fourth European working conditions survey. Luxembourg: Office for Official Publications of the European Communities; 2007.
McMenamin TM. A time to work: recent trends in shift work and flexible schedules. Mon Labor Rev. 2007;130:3–15.
Knutsson A, Alfredsson L, Karlsson B, et al. Breast cancer among shift workers: results of the WOLF longitudinal cohort study. Scand J Work Environ Health. 2013;39(2):170–7.
Koppes LL, Geuskens GA, Pronk A, Vermeulen RC, de Vroome EM. Night work and breast cancer risk in a general population prospective cohort study in the Netherlands. Eur J Epidemiol. 2014;29:577–84.
Gu F, Han J, Laden F, et al. Total and cause-specific mortality of U.S. nurses working rotating night shifts. Am J Prev Med. 2015;48:241–52.
Akerstedt T, Knutsson A, Narusyte J, Svedberg P, Kecklund G, Alexanderson K. Night work and breast cancer in women: a Swedish cohort study. BMJ Open. 2015;5(4):e008127.
Lie JA, Kjuus H, Zienolddiny S, Haugen A, Stevens RG, Kjaerheim K. Night work and breast cancer risk among Norwegian nurses: assessment by different exposure metrics. Am J Epidemiol. 2011;173:1272–9.
Hansen J, Lassen CF. Nested case-control study of night shift work and breast cancer risk among women in the Danish military. Occup Environ Med. 2012;69:551–6.
Hansen J, Stevens RG. Case-control study of shift-work and breast cancer risk in Danish nurses: impact of shift systems. Eur J Cancer. 2012;48:1722–9.
Menegaux F, Truong T, Anger A, et al. Night work and breast cancer: a population-based case-control study in France (the CECILE study). Int J Cancer. 2013;132:924–31.
Rabstein S, Harth V, Pesch B, et al. Night work and breast cancer estrogen receptor status-results from the German GENICA study. Scand J Work Environ Health. 2013;39(5):448–55.
Fritschi L, Erren TC, Glass DC, et al. The association between different night shiftwork factors and breast cancer: a case-control study. Br J Cancer. 2013;109:2472–80.
Grundy A, Richardson H, Burstyn I, et al. Increased risk of breast cancer associated with long-term shift work in Canada. Occup Environ Med. 2013;70:831–8.
Li W, Ray RM, Thomas DB, et al. Shift work and breast cancer among women textile workers in Shanghai, China. Cancer Causes Control. 2015;26:143–50.
Wang P, Ren FM, Lin Y, et al. Night-shift work, sleep duration, daytime napping, and breast cancer risk. Sleep Med. 2015;16:462–8.
Papantoniou K, Castano-Vinyals G, Espinosa A, et al. Breast cancer risk and night shift work in a case-control study in a Spanish population. Eur J Epidemiol. 2016;31:867–78.
Wegrzyn LR, Tamimi RM, Rosner BA, et al. Rotating night-shift work and the risk of breast cancer in the Nurses’ Health studies. Am J Epidemiol. 2017;186:532–40.
ANSES. Opinion of the French Agency for Food, Environmental and Occupational Health & Safety on the “Assessment of the health risks associated with night work”. Request No 2011-SA-0088. May 2016. https://www.anses.fr/fr/system/files/AP2011SA0088EN.pdf.
ANSES (Agence nationale de sécurité sanitaire de l’alimentation, de l’environnement et du travail). Évaluation des risques sanitaires liés au travail de nuit. Avis de l’Anses et Rapport d’expertise collective. Maisons-Alfort: ANSES; 2016. 408 p. https://www.anses.fr/fr/system/files/AP2011SA0088Ra.pdf.
Ijaz S, Verbeek J, Seidler A, et al. Night-shift work and breast cancer—a systematic review and meta-analysis. Scand J Work Environ Health. 2013;39:431–47.
Jia Y, Lu Y, Wu K, et al. Does night work increase the risk of breast cancer? A systematic review and meta-analysis of epidemiological studies. Cancer Epidemiol. 2013;37:197–206.
Kamdar BB, Tergas AI, Mateen FJ, Bhayani NH, Oh J. Night-shift work and risk of breast cancer: a systematic review and meta-analysis. Breast Cancer Res Treat. 2013;138:291–301.
Wang F, Yeung KL, Chan WC, et al. A meta-analysis on dose-response relationship between night shift work and the risk of breast cancer. Ann Oncol. 2013;24:2724–32.
He C, Anand ST, Ebell MH, Vena JE, Robb SW. Circadian disrupting exposures and breast cancer risk: a meta-analysis. Int Arch Occup Environ Health. 2015;88:533–47.
Lin X, Chen W, Wei F, Ying M, Wei W, Xie X. Night-shift work increases morbidity of breast cancer and all-cause mortality: a meta-analysis of 16 prospective cohort studies. Sleep Med. 2015;16:1381–7.
Travis RC, Balkwill A, Fensom GK, et al. Night shift work and breast cancer incidence: three prospective studies and meta-analysis of published studies. J Natl Cancer Inst. 2016;108(12):djw169.
Stevens RG. Light-at-night, circadian disruption and breast cancer: assessment of existing evidence. Int J Epidemiol. 2009;38:963–70.
Schernhammer ES, Hankinson SE. Urinary melatonin levels and breast cancer risk. J Natl Cancer Inst. 2005;97:1084–7.
Schernhammer ES, Rosner B, Willett WC, Laden F, Colditz GA, Hankinson SE. Epidemiology of urinary melatonin in women and its relation to other hormones and night work. Cancer Epidemiol Biomark Prev. 2004;13:936–43.
Travis RC, Allen DS, Fentiman IS, Key TJ. Melatonin and breast cancer: a prospective study. J Natl Cancer Inst. 2004;96:475–82.
Wang JX, Zhang LA, Li BX, et al. Cancer incidence and risk estimation among medical x-ray workers in China, 1950-1995. Health Phys. 2002;82:455–66.
Doody MM, Freedman DM, Alexander BH, et al. Breast cancer incidence in U.S. radiologic technologists. Cancer. 2006;106:2707–15.
Linet MS, Hauptmann M, Freedman DM, et al. Interventional radiography and mortality risks in U.S. radiologic technologists. Pediatr Radiol. 2006;36(Suppl 2):113–20.
McGeoghegan D, Binks K. The mortality and cancer morbidity experience of workers at the Springfields uranium production facility, 1946–95. J Radiol Prot. 2000;20:111–37.
Telle-Lamberton M, Bergot D, Gagneau M, et al. Cancer mortality among French atomic energy commission workers. Am J Ind Med. 2004;45:34–44.
Shaham J, Gurvich R, Goral A, Czerniak A. The risk of breast cancer in relation to health habits and occupational exposures. Am J Ind Med. 2006;49:1021–30.
Sont WN, Zielinski JM, Ashmore JP, et al. First analysis of cancer incidence and occupational radiation exposure based on the National Dose Registry of Canada. Am J Epidemiol. 2001;153:309–18.
Ashmore JP, Krewski D, Zielinski JM, Jiang H, Semenciw R, Band PR. First analysis of mortality and occupational radiation exposure based on the National Dose Registry of Canada. Am J Epidemiol. 1998;148:564–74.
McGeoghegan D, Binks K. The mortality and cancer morbidity experience of workers at the Capenhurst uranium enrichment facility 1946–95. J Radiol Prot. 2000;20:381–401.
McGeoghegan D, Gillies M, Riddell AE, Binks K. Mortality and cancer morbidity experience of female workers at the British nuclear fuels sellafield plant, 1946–1998. Am J Ind Med. 2003;44:653–63.
Silver SR, Whelan EA, Deddens JA, et al. Occupational exposure to polychlorinated biphenyls and risk of breast cancer. Environ Health Perspect. 2009;117(2):276–82.
Ruder AM, Hein MJ, Hopf NB, Waters MA. Mortality among 24,865 workers exposed to polychlorinated biphenyls (PCBs) in three electrical capacitor manufacturing plants: a ten-year update. Int J Hyg Environ Health. 2014;217:176–87.
Engel LS, Werder E, Satagopan J, et al. Insecticide use and breast cancer risk among farmers’ wives in the Agricultural Health Study. Environ Health Perspect. 2017;125:097002.
Louis LM, Lerro CC, Friesen MC, et al. A prospective study of cancer risk among Agricultural Health Study farm spouses associated with personal use of organochlorine insecticides. Environ Health. 2017;16:95.
Rennix CP, Quinn MM, Amoroso PJ, Eisen EA, Wegman DH. Risk of breast cancer among enlisted army women occupationally exposed to volatile organic compounds. Am J Ind Med. 2005;48:157–67.
Sung TI, Chen PC, Jyuhn-Hsiarn LL, Lin YP, Hsieh GY, Wang JD. Increased standardized incidence ratio of breast cancer in female electronics workers. BMC Public Health. 2007;7:102.
Peplonska B, Stewart P, Szeszenia-Dabrowska N, et al. Occupational exposure to organic solvents and breast cancer in women. Occup Environ Med. 2010;67:722–9.
Labreche F, Goldberg MS, Valois MF, Nadon L. Postmenopausal breast cancer and occupational exposures. Occup Environ Med. 2010;67:263–9.
Hansen J. Breast cancer risk among relatively young women employed in solvent-using industries. Am J Ind Med. 1999;36:43–7.
Band PR, Le ND, Fang R, Deschamps M, Gallagher RP, Yang P. Identification of occupational cancer risks in British Columbia. A population-based case-control study of 995 incident breast cancer cases by menopausal status, controlling for confounding factors. J Occup Environ Med. 2000;42:284–310.
Peplonska B, Stewart P, Szeszenia-Dabrowska N, et al. Occupation and breast cancer risk in Polish women: a population-based case-control study. Am J Ind Med. 2007;50:97–111.
Chang YM, Tai CF, Yang SC, et al. A cohort mortality study of workers exposed to chlorinated organic solvents in Taiwan. Ann Epidemiol. 2003;13:652–60.
McElvenny DM, Darnton AJ, Hodgson JT, Clarke SD, Elliott RC, Osman J. Investigation of cancer incidence and mortality at a Scottish semiconductor manufacturing facility. Occup Med (Lond). 2003;53:419–30.
Boffetta P, Adami HO, Cole P, Trichopoulos D, Mandel JS. Epidemiologic studies of styrene and cancer: a review of the literature. J Occup Environ Med. 2009;51:1275–87.
Costantini AS, Gorini G, Consonni D, Miligi L, Giovannetti L, Quinn M. Exposure to benzene and risk of breast cancer among shoe factory workers in Italy. Tumori. 2009;95:8–12.
Petralia SA, Vena JE, Freudenheim JL, et al. Risk of premenopausal breast cancer in association with occupational exposure to polycyclic aromatic hydrocarbons and benzene. Scand J Work Environ Health. 1999;25:215–21.
Pukkala E, Martinsen JI, Lynge E, et al. Occupation and cancer—follow-up of 15 million people in five Nordic countries. Acta Oncol. 2009;48:646–790.
Villeneuve S, Fevotte J, Anger A, et al. Breast cancer risk by occupation and industry: analysis of the CECILE study, a population-based case-control study in France. Am J Ind Med. 2011;54:499–509.
Forssen UM, Rutqvist LE, Ahlbom A, Feychting M. Occupational magnetic fields and female breast cancer: a case-control study using Swedish population registers and new exposure data. Am J Epidemiol. 2005;161:250–9.
McElroy JA, Egan KM, Titus-Ernstoff L, et al. Occupational exposure to electromagnetic field and breast cancer risk in a large, population-based, case-control study in the United States. J Occup Environ Med. 2007;49:266–74.
Gardner KM, Ou SX, Jin F, et al. Occupations and breast cancer risk among Chinese women in urban Shanghai. Am J Ind Med. 2002;42:296–308.
Labreche F, Goldberg MS, Valois MF, et al. Occupational exposures to extremely low frequency magnetic fields and postmenopausal breast cancer. Am J Ind Med. 2003;44:643–52.
Van Wijngaarden E, Nylander-French LA, Millikan RC, Savitz DA, Loomis D. Population-based case-control study of occupational exposure to electromagnetic fields and breast cancer. Ann Epidemiol. 2001;11:297–303.
Hansen J, Olsen JH, Larsen AI. Cancer morbidity among employees in a Danish pharmaceutical plant. Int J Epidemiol. 1994;23:891–8.
Edling C, Friis L, Mikoczy Z, Hagmar L, Lindfors P. Cancer incidence among pharmaceutical workers. Scand J Work Environ Health. 1995;21:116–23.
Harrington JM, Goldblatt P. Census based mortality study of pharmaceutical industry workers. Br J Ind Med. 1986;43:206–11.
Hansen J, Olsen JH. Cancer morbidity among Danish female pharmacy technicians. Scand J Work Environ Health. 1994;20:22–6.
Shaham J, Gurvich R, Kneshet Y. Cancer incidence among laboratory workers in biomedical research and routine laboratories in Israel: part II-nested case-control study. Am J Ind Med. 2003;44:611–26.
Gustavsson P, Andersson T, Gustavsson A, Reuterwall C. Cancer incidence in female laboratory employees: extended follow-up of a Swedish cohort study. Occup Environ Med. 2017;74:823–6.
Brophy JT, Keith MM, Gorey KM, et al. Occupation and breast cancer: a Canadian case-control study. Ann N Y Acad Sci. 2006;1076:765–77.
Pinkerton LE, Hein MJ, Stayner LT. Mortality among a cohort of garment workers exposed to formaldehyde: an update. Occup Environ Med. 2004;61(3):193–200.
Rafnsson V, Sulem P, Tulinius H, Hrafnkelsson J. Breast cancer risk in airline cabin attendants: a nested case-control study in Iceland. Occup Environ Med. 2003;60:807–9.
Linnersjo A, Hammar N, Dammstrom BG, Johansson M, Eliasch H. Cancer incidence in airline cabin crew: experience from Sweden. Occup Environ Med. 2003;60:810–4.
Haldorsen T, Reitan JB, Tveten U. Cancer incidence among Norwegian airline cabin attendants. Int J Epidemiol. 2001;30:825–30.
Zeeb H, Blettner M, Langner I, et al. Mortality from cancer and other causes among airline cabin attendants in Europe: a collaborative cohort study in eight countries. Am J Epidemiol. 2003;158:35–46.
Kojo K, Pukkala E, Auvinen A. Breast cancer risk among Finnish cabin attendants: a nested case-control study. Occup Environ Med. 2005;62:488–93.
Clapp RW, Hoffman K. Cancer mortality in IBM Endicott plant workers, 1969–2001: an update on a NY production plant. Environ Health. 2008;7:13.
MacArthur AC, Le ND, Abanto ZU, Gallagher RP. Occupational female breast and reproductive cancer mortality in British Columbia, Canada, 1950–94. Occup Med (Lond). 2007;57:246–53.
Quach T, Doan-Billing PA, Layefsky M, et al. Cancer incidence in female cosmetologists and manicurists in California, 1988–2005. Am J Epidemiol. 2010;172:691–9.
United Nations Scientific Committee on the Effects of Atomic Radiation. Sources and effects of ionizing radiation. UNSCEAR 2008 report to the general assembly with scientific annexes, vol. 1. New York: United Nations; 2010.
Wang F-R, Fang Q-Q, Tang W-M, et al. Nested case-control study of occupational radiation exposure and breast and esophagus cancer risk among medical diagnostic X Ray Workers in Jiangsu of China. Asian Pac J Cancer Prev. 2015;16:4699–704.
Preston DL, Kitahara CM, Freedman DM, et al. Breast cancer risk and protracted low-to-moderate dose occupational radiation exposure in the US Radiologic Technologists Cohort, 1983-2008. Br J Cancer. 2016;115:1105–12.
Yoshinaga S, Mabuchi K, Sigurdson AJ, Doody MM, Ron E. Cancer risks among radiologists and radiologic technologists: review of epidemiologic studies. Radiology. 2004;233:313–21.
Linet MS, Kim KP, Miller DL, Kleinerman RA, Simon SL, Berrington de Gonzalez A. Historical review of occupational exposures and cancer risks in medical radiation workers. Radiat Res. 2010;174:793–808.
Boice JD Jr, Cohen SS, Mumma MT, Chadda B, Blot WJ. A cohort study of uranium millers and miners of Grants, New Mexico, 1979-2005. J Radiol Prot. 2008;28(3):303–25.
Samson E, Piot I, Zhivin S, et al. Cancer and non-cancer mortality among French uranium cycle workers: the TRACY cohort. BMJ Open. 2016;6(4):e010316.
Buitenhuis W, Fritschi L, Thomson A, Glass D, Heyworth J, Peters S. Occupational exposure to ionizing radiation and risk of breast cancer in Western Australia. J Occup Environ Med. 2013;55:1431–5.
Sont WN, Zielinski JM, Ashmore JP, et al. Sont et al. Respond to “studies of workers exposed to low doses of radiation”. Am J Epidemiol. 2001;153:323–4.
Ruder AM, Hein MJ, Hopf NB, Waters MA. Cancer incidence among capacitor manufacturing workers exposed to polychlorinated biphenyls. Am J Ind Med. 2017;60:198–207.
Guyton KZ, Loomis D, Grosse Y, et al. Carcinogenicity of pentachlorophenol and some related compounds. Lancet Oncol. 2016;17:1637–8.
Han Y, Mo R, Yuan X, et al. Pesticide residues in nut-planted soils of China and their relationship between nut/soil. Chemosphere. 2017;180:42–7.
Gevao B, Porcelli M, Rajagopalan S, et al. Spatial and temporal variations in the atmospheric concentrations of “Stockholm Convention” organochlorine pesticides in Kuwait. Sci Total Environ. 2018;622–623:1621–9. pii: S0048-9697(17)32737–7.
Dang VD, Kroll KJ, Supowit SD, Halden RU, Denslow ND. Tissue distribution of organochlorine pesticides in largemouth bass (Micropterus salmoides) from laboratory exposure and a contaminated lake. Environ Pollut. 2016;216:877–8.
Campillo JA, Fernandez B, Garcia V, Benedicto J, Leon VM. Levels and temporal trends of organochlorine contaminants in mussels from Spanish Mediterranean waters. Chemosphere. 2017;182:584–94.
Høyer AP, Grandjean P, Jørgensen T, Brock JW, Hartvig HB. Organochlorine exposure and risk of breast cancer. Lancet. 1998;352:1816–20.
Gammon MD, Wolff MS, Neugut AI, et al. Environmental toxins and breast cancer on Long Island. II. Organochlorine compound levels in blood. Cancer Epidemiol Biomarkers Prev. 2002;11:686–97.
Ward EM, Schulte P, Grajewski B, et al. Serum organochlorine levels and breast cancer: a nested case-control study of Norwegian women. Cancer Epidemiol Biomarkers Prev. 2000;9:1357–67.
IARC. Monographs on the evaluation on carcinogenic risks to humans. Some drugs and herbal products, vol. 108. Lyon: International Agency for Research on Cancer; 2016.
Connor TH, McDiarmid MA. Preventing occupational exposures to antineoplastic drugs in health care settings. CA Cancer J Clin. 2006;56:354–65.
Heron RJ, Pickering FC. Health effects of exposure to Active Pharmaceutical Ingredients (APIs). Occup Med (Lond). 2003;53:357–62.
Thomas TL, Decoufle P. Mortality among workers employed in the pharmaceutical industry: a preliminary investigation. J Occup Med. 1979;21:619–23.
Baker CC, Russell RA, Roder DM, Esterman AJ. A nine year retrospective mortality study of workers in a British pharmaceutical company. J Soc Occup Med. 1986;36:95–8.
Ekenga CC, Parks CG, D’Aloisio AA, Deroo LA, Sandler DP. Breast cancer risk after occupational solvent exposure: the influence of timing and setting. Cancer Res. 2014;74(11):3076–83.
IARC. Monographs on the evaluation on carcinogenic risks to humans. Some non-heterocyclic polycyclic aromatic hydrocarbons and some related exposures, vol. 92. Lyon: International Agency for Research on Cancer; 2010.
Rai R, Glass DC, Heyworth JS, Saunders C, Fritschi L. Occupational exposures to engine exhausts and other PAHs and breast cancer risk: a population-based case-control study. Am J Ind Med. 2016;59:437–44.
Jeffy BD, Chirnomas RB, Romagnolo DF. Epigenetics of breast cancer: polycyclic aromatic hydrocarbons as risk factors. Environ Mol Mutagen. 2002;39:235–44.
de Vocht F, Sobala W, Wilczynska U, Kromhout H, Szeszenia-Dabrowska N, Peplonska B. Cancer mortality and occupational exposure to aromatic amines and inhalable aerosols in rubber tire manufacturing in Poland. Cancer Epidemiol. 2009;33:94–102.
Rabstein S, Bruning T, Harth V, et al. N-acetyltransferase 2, exposure to aromatic and heterocyclic amines, and receptor-defined breast cancer. Eur J Cancer Prev. 2010;19:100–9.
Thompson D, Kriebel D, Quinn MM, Wegman DH, Eisen EA. Occupational exposure to metalworking fluids and risk of breast cancer among female autoworkers. Am J Ind Med. 2005;47:153–60.
Caplan LS, Schoenfeld ER, O’Leary ES, Leske MC. Breast cancer and electromagnetic fields—a review. Ann Epidemiol. 2000;10:31–44.
IARC. Monographs on the evaluation on carcinogenic risks to humans. Non-ionizing radiation. Part 1: static and extremely low-frequency (ELF) electric and magnetic fields, vol. 80. Lyon: International Agency for Research on Cancer; 2002.
Goodman M, Kelsh M, Ebi K, Iannuzzi J, Langholz B. Evaluation of potential confounders in planning a study of occupational magnetic field exposure and female breast cancer. Epidemiology. 2002;13:50–8.
Ahlbom IC, Cardis E, Green A, Linet M, Savitz D, Swerdlow A. Review of the epidemiologic literature on EMF and Health. Environ Health Perspect. 2001;109(Suppl 6):911–33.
Johansen C. Electromagnetic fields and health effects–epidemiologic studies of cancer, diseases of the central nervous system and arrhythmia-related heart disease. Scand J Work Environ Health. 2004;30(Suppl 1):1–30.
Feychting M, Forssen U. Electromagnetic fields and female breast cancer. Cancer Causes Control. 2006;17:553–8.
Engel LS, Hill DA, Hoppin JA, et al. Pesticide use and breast cancer risk among farmers’ wives in the agricultural health study. Am J Epidemiol. 2005;161:121–35.
Salehi F, Turner MC, Phillips KP, Wigle DT, Krewski D, Aronson KJ. Review of the etiology of breast cancer with special attention to organochlorines as potential endocrine disruptors. J Toxicol Environ Health B Crit Rev. 2008;11:276–300.
Manuwald U, Velasco GM, Berger J, Manz A, Baur X. Mortality study of chemical workers exposed to dioxins: follow-up 23 years after chemical plant closure. Occup Environ Med. 2012;69:636–42.
Brody JG, Moysich KB, Humblet O, Attfield KR, Beehler GP, Rudel RA. Environmental pollutants and breast cancer: epidemiologic studies. Cancer. 2007;109(Suppl 12):2667–711.
McCready D, Aronson KJ, Chu W, Fan W, Vesprini D, Narod SA. Breast tissue organochlorine levels and metabolic genotypes in relation to breast cancer risk Canada. Cancer Causes Control. 2004;15:399–418.
Franco G. Bernardino Ramazzini and women workers’ health in the second half of the XVIIth century. J Public Health (Oxf). 2012;34:305–8.
Goldberg MS, Labreche F. Occupational risk factors for female breast cancer: a review. Occup Environ Med. 1996;53:145–56.
Carpenter L, Roman E. Cancer and occupation in women: identifying associations using routinely collected national data. Environ Health Perspect. 1999;107(Suppl 2):299–303.
Bernstein L, Allen M, Anton-Culver H, et al. High breast cancer incidence rates among California teachers: results from the California teachers study (United States). Cancer Causes Control. 2002;13:625–35.
Teitelbaum SL, Britton JA, Gammon MD, et al. Occupation and breast cancer in women 20–44 years of age (United States). Cancer Causes Control. 2003;14:627–37.
Kullberg C, Selander J, Albin M, Borgquist S, Manjer J, Gustavsson P. Female white-collar workers remain at higher risk of breast cancer after adjustments for individual risk factors related to reproduction and lifestyle. Occup Environ Med. 2017;74(9):652–8.
Larsen SB, Olsen A, Lynch J, et al. Socioeconomic position and lifestyle in relation to breast cancer incidence among postmenopausal women: a prospective cohort study, Denmark, 1993–2006. Cancer Epidemiol. 2011;35:438–41.
Oddone E, Edefonti V, Scaburri A, Vai T, Crosignani P, Imbriani M. Female breast cancer in Lombardy, Italy (2002-2009): a case-control study on occupational risks. Am J Ind Med. 2013;56(9):1051–62.
Simning A, Van WE. Literature review of cancer mortality and incidence among dentists. Occup Environ Med. 2007;64:432–8.
Nichols L, Sorahan T. Mortality of UK electricity generation and transmission workers, 1973–2002. Occup Med (Lond). 2005;55:541–8.
Brophy JT, Keith MM, Watterson A, et al. Breast cancer risk in relation to occupations with exposure to carcinogens and endocrine disruptors: a Canadian case-control study. Environ Health. 2012;11:87.
Colt JS, Stallones L, Cameron LL, Dosemeci M, Zahm SH. Proportionate mortality among US migrant and seasonal farmworkers in twenty-four states. Am J Ind Med. 2001;40:604–11.
Nanni O, Ravaioli A, Bucchi L, et al. Relative and absolute cancer mortality of women in agriculture in Northern Italy. Eur J Cancer Prev. 2005;14:337–444.
Mills PK, Shah P. Cancer incidence in California farm workers, 1988-2010. Am J Ind Med. 2014;57(7):737–47.
Whelan EA. Cancer incidence in airline cabin crew. Occup Environ Med. 2003;60:805–6.
Schubauer-Berigan MK, Anderson JL, Hein MJ, Little MP, Sigurdson AJ, Pinkerton LE. Breast cancer incidence in a cohort of U.S. flight attendants. Am J Ind Med. 2015;58:252–66.
Pinkerton LE, Hein MJ, Anderson JL, Little MP, Sigurdson AJ, Schubauer-Berigan MK. Breast cancer incidence among female flight attendants: exposure-response analyses. Scand J Work Environ Health. 2016;42:538–46.
Coyle YM. The effect of environment on breast cancer risk. Breast Cancer Res Treat. 2004;84:273–88.
Jablonska E, Socha K, Reszka E, et al. Cadmium, arsenic, selenium and iron–implications for tumor progression in breast cancer. Environ Toxicol Pharmacol. 2017;53:151–7.
Lewis-Michl EL, Melius JM, Kallenbach LR, et al. Breast cancer risk and residence near industry or traffic in Nassau and Suffolk Counties, Long Island, New York. Arch Environ Health. 1996;51:255–65.
Bonner MR, Han D, Nie J, et al. Breast cancer risk and exposure in early life to polycyclic aromatic hydrocarbons using total suspended particulates as a proxy measure. Cancer Epidemiol Biomarkers Prev. 2005;14:53–60.
Nie J, Beyea J, Bonner MR, et al. Exposure to traffic emissions throughout life and risk of breast cancer: the Western New York Exposures and Breast Cancer (WEB) study. Cancer Causes Control. 2007;18:947–55.
Hart JE, Bertrand KA, DuPre N, et al. Long-term particulate matter exposures during adulthood and risk of breast cancer incidence in the Nurses’ Health Study II Prospective Cohort. Cancer Epidemiol Biomarkers Prev. 2016;25:1274–6.
Reding KW, Young MT, Szpiro AA, et al. Breast cancer risk in relation to ambient air pollution exposure at residences in the sister study cohort. Cancer Epidemiol Biomarkers Prev. 2015;24:1907–9.
Crouse DL, Goldberg MS, Ross NA, Chen H, Labreche F. Postmenopausal breast cancer is associated with exposure to traffic-related air pollution in Montreal, Canada: a case-control study. Environ Health Perspect. 2010;118:1578–83.
Goldberg MS, Labrèche F, Weichenthal S, et al. The association between the incidence of postmenopausal breast cancer and concentrations at street-level of nitrogen dioxide and ultrafine particles. Environ Res. 2017;158:7–15.
Hystad P, Villeneuve PJ, Goldberg MS, Crouse DL, Johnson K. Exposure to traffic-related air pollution and the risk of developing breast cancer among women in eight Canadian provinces: a case-control study. Environ Int. 2015;74:240–8.
Rothman N, Wacholder S, Caporaso NE, Garcia-Closas M, Buetow K, Fraumeni JF Jr. The use of common genetic polymorphisms to enhance the epidemiologic study of environmental carcinogens. Biochim Biophys Acta. 2001;1471:C1–10.
Masson LF, Sharp L, Cotton SC, Little J. Cytochrome P-450 1A1 gene polymorphisms and risk of breast cancer: a HuGE review. Am J Epidemiol. 2005;161:901–15.
Rihs HP, Pesch B, Kappler M, et al. Occupational exposure to polycyclic aromatic hydrocarbons in German industries: association between exogenous exposure and urinary metabolites and its modulation by enzyme polymorphisms. Toxicol Lett. 2005;157:241–55.
Zhang Y, Wise JP, Holford TR, et al. Serum polychlorinated biphenyls, cytochrome P-450 1A1 polymorphisms, and risk of breast cancer in Connecticut women. Am J Epidemiol. 2004;160:1177–83.
Moysich KB, Shields PG, Freudenheim JL, et al. Polychlorinated biphenyls, cytochrome P4501A1 polymorphism, and postmenopausal breast cancer risk. Cancer Epidemiol Biomarkers Prev. 1999;8:41–4.
Laden F, Ishibe N, Hankinson SE, et al. Polychlorinated biphenyls, cytochrome P450 1A1, and breast cancer risk in the nurses’ health study. Cancer Epidemiol Biomarkers Prev. 2002;11:1560–5.
Surekha D, Sailaja K, Rao DN, Padma T, Raghunadharao D, Vishnupriya S. Association of CYP1A1∗2 polymorphisms with breast cancer risk: a case control study. Indian J Med Sci. 2009;63:13–20.
Chang-Claude J, Kropp S, Jager B, Bartsch H, Risch A. Differential effect of NAT2 on the association between active and passive smoke exposure and breast cancer risk. Cancer Epidemiol Biomarkers Prev. 2002;11:698–704.
Terry PD, Goodman M. Is the association between cigarette smoking and breast cancer modified by genotype? A review of epidemiologic studies and meta-analysis. Cancer Epidemiol Biomarkers Prev. 2006;15:602–11.
Conlon MS, Johnson KC, Bewick MA, Lafrenie RM, Donner A. Smoking (active and passive), N-acetyltransferase 2, and risk of breast cancer. Cancer Epidemiol. 2010;34:142–9.
Mitrunen K, Jourenkova N, Kataja V, et al. Glutathione S-transferase M1, M3, P1, and T1 genetic polymorphisms and susceptibility to breast cancer. Cancer Epidemiol Biomarkers Prev. 2001;10:229–36.
Park SK, Yoo KY, Lee SJ, et al. Alcohol consumption, glutathione S-transferase M1 and T1 genetic polymorphisms and breast cancer risk. Pharmacogenetics. 2000;10:301–9.
Helzlsouer KJ, Selmin O, Huang HY, et al. Association between glutathione S-transferase M1, P1, and T1 genetic polymorphisms and development of breast cancer. J Natl Cancer Inst. 1998;90:512–8.
Sturmer T, Wang-Gohrke S, Arndt V, et al. Interaction between alcohol dehydrogenase II gene, alcohol consumption, and risk for breast cancer. Br J Cancer. 2002;87:519–23.
Barrdahl M, Rudolph A, Hopper JL, et al. Gene-environment interactions involving functional variants: results from the breast Cancer Association Consortium. Int J Cancer. 2017;141:1830–40.
Iarmarcovai G, Bonassi S, Botta A, Baan RA, Orsiere T. Genetic polymorphisms and micronucleus formation: a review of the literature. Mutat Res. 2008;658:215–33.
Furberg H, Millikan RC, Geradts J, et al. Environmental factors in relation to breast cancer characterized by p53 protein expression. Cancer Epidemiol Biomarkers Prev. 2002;11:829–35.
Nurminen M, Karjalainen A. Epidemiologic estimate of the proportion of fatalities related to occupational factors in Finland. Scand J Work Environ Health. 2001;27:161–213.
Slack R, Young C, Rushton L. Occupational cancer in Britain—female cancers: breast, cervix and ovary. Br J Cancer. 2012;107(Suppl 1):S27–32.
Purdue MP, Hutchings SJ, Rushton L, Silverman DT. The proportion of cancer attributable to occupational exposures. Ann Epidemiol. 2015;25:188–92.
Carey RN, Hutchings SJ, Rushton L, et al. The future excess fraction of occupational cancer among those exposed to carcinogens at work in Australia in 2012. Cancer Epidemiol. 2017;47:1–6.
Forman D, Bray F, Brewster DH, et al., editors. Cancer incidence in five continents, vol. X. IARC Scientific Publication No. 164. Lyon: International Agency for Research on Cancer; 2014. http://ci5.iarc.fr/CI5I-X/Default.aspx. Accessed 31 July 2017.
Gatta G, van der Zwan JM, Casali PG, et al. Rare cancers are not so rare: the rare cancer burden in Europe. Eur J Cancer. 2011;47:2493–511.
Stang A, Thomssen C. Decline in breast cancer incidence in the United States: what about male breast cancer? Breast Cancer Res Treat. 2008;112:595–6.
Contractor KB, Kaur K, Rodrigues GS, Kulkarni DM, Singhal H. Male breast cancer: is the scenario changing. World J Surg Oncol. 2008;6:58.
Miao H, Verkooijen H, Chia KS, et al. Incidence and outcome of male breast cancer: an international population-based study. J Clin Oncol. 2011;29:4381–6.
Weiss JR, Moysich KB, Swede H. Epidemiology of male breast cancer. Cancer Epidemiol Biomarkers Prev. 2005;14:20–6.
Ottini L, Palli D, Rizzo S, Federico M, Bazan V, Russo A. Male breast cancer. Crit Rev Oncol Hematol. 2010;73:141–55.
Ewertz M, Holmberg L, Tretli S, Pedersen BV, Kristensen A. Risk factors for male breast cancer—a case-control study from Scandinavia. Acta Oncol. 2001;40:467–71.
Guenel P, Cyr D, Sabroe S, et al. Alcohol drinking may increase risk of breast cancer in men: a European population-based case-control study. Cancer Causes Control. 2004;15:571–80.
Lynge E, Afonso N, Kaerlev L, et al. European multi-centre case-control study on risk factors for rare cancers of unknown aetiology. Eur J Cancer. 2005;41:601–12.
Fentiman IS, Fourquet A, Hortobagyi GN. Male breast cancer. Lancet. 2006;367:595–604.
Thomas DB, Rosenblatt K, Jimenez LM, et al. Ionizing radiation and breast cancer in men (United States). Cancer Causes Control. 1994;5:9–14.
Little MP, McElvenny DM. Male breast cancer incidence and mortality risk in the Japanese atomic bomb survivors—differences in excess relative and absolute risk from female breast cancer. Environ Health Perspect. 2017;125:223–9.
Charbotel B, Fervers B, Droz JP. Occupational exposures in rare cancers: a critical review of the literature. Crit Rev Oncol Hematol. 2014;90:99–134.
Pollan M, Gustavsson P, Floderus B. Breast cancer, occupation, and exposure to electromagnetic fields among Swedish men. Am J Ind Med. 2001;39:276–85.
Sun JW, Li XR, Gao HY, et al. Electromagnetic field exposure and male breast cancer risk: a meta-analysis of 18 studies. Asian Pac J Cancer Prev. 2013;14:523–8.
Hansen J. Elevated risk for male breast cancer after occupational exposure to gasoline and vehicular combustion products. Am J Ind Med. 2000;37:349–52.
Cocco P, Figgs L, Dosemeci M, Hayes R, Linet MS, Hsing AW. Case-control study of occupational exposures and male breast cancer. Occup Environ Med. 1998;55:599–604.
Kimbrough RD, Krouskas CA, Xu W, Shields PG. Mortality among capacitor workers exposed to polychlorinated biphenyls (PCBs), a long-term update. Int Arch Occup Environ Health. 2015;88:85–101.
Mabuchi K, Bross DS, Kessler II. Risk factors for male breast cancer. J Natl Cancer Inst. 1985;74:371–5.
Lenfant-Pejovic MH, Mlika-Cabanne N, Bouchardy C, Auquier A. Risk factors for male breast cancer: a Franco-Swiss case-control study. Int J Cancer. 1990;45:661–5.
Rosenbaum PF, Vena JE, Zielezny MA, Michalek AM. Occupational exposures associated with male breast cancer. Am J Epidemiol. 1994;139:30–6.
Kaplan SD. Retrospective cohort mortality study of Roman Catholic priests. Prev Med. 1988;17:335–43.
Rigoni S. Statistical facts about cancers on which Doctor Rigoni-Stern based his contribution to the Surgeons’ Subgroup of the IV Congress of the Italian Scientists on 23 September 1842. (translation). Stat Med. 1987;6:881–4.
Fritschi L, Guenel P, Ahrens W. Breast cancer in priests: follow-up of an observation made 167 years ago. Eur J Epidemiol. 2010;25:219–21.
Swaen GM, Burns C, Teta JM, Bodner K, Keenan D, Bodnar CM. Mortality study update of ethylene oxide workers in chemical manufacturing: a 15 year update. J Occup Environ Med. 2009;51:714–23.
Wirth M, Vena JE, Smith EK, Bauer SE, Violanti J, Burch J. The epidemiology of cancer among police officers. Am J Ind Med. 2013;56:439–53.
Ma F, Fleming LE, Lee DJ, et al. Mortality in Florida professional firefighters, 1972 to 1999. Am J Ind Med. 2005;47:509–17.
Glass DC, Pircher S, Del Monaco A, Hoorn SV, Sim MR. Mortality and cancer incidence in a cohort of male paid Australian firefighters. Occup Environ Med. 2016;73:761–71.
Ma F, Fleming LE, Lee DJ, Trapido E, Gerace TA. Cancer incidence in Florida professional firefighters, 1981 to 1999. J Occup Environ Med. 2006;48:883–8.
Daniels RD, Kubale TL, Yiin JH, et al. Mortality and cancer incidence in a pooled cohort of US firefighters from San Francisco, Chicago and Philadelphia (1950-2009). Occup Environ Med. 2014;71:388–97.
Villeneuve S, Cyr D, Lynge E, et al. Occupation and occupational exposure to endocrine disrupting chemicals in male breast cancer: a case-control study in Europe. Occup Environ Med. 2010;67:837–44.
Palli D, Masala G, Mariani-Costantini R, et al. A gene-environment interaction between occupation and BRCA1/BRCA2 mutations in male breast cancer? Eur J Cancer. 2004;40:2474–9.
Nilsson C, Holmqvist M, Bergkvist L, Hedenfalk I, Lambe M, Fjallskog ML. Similarities and differences in the characteristics and primary treatment of breast cancer in men and women—a population based study (Sweden). Acta Oncol. 2011;50:1083–8.
Disclaimer
Where authors are identified as personnel of the International Agency for Research on Cancer/World Health Organization, the authors alone are responsible for the views expressed in this article and they do not necessarily represent the decisions, policy or views of the International Agency for Research on Cancer/World Health Organization. Dr. Hashim was at IARC at the time of writing this chapter.
Author information
Authors and Affiliations
Corresponding author
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2020 Springer Nature Switzerland AG
About this chapter
Cite this chapter
Labrèche, F., Goldberg, M.S., Hashim, D., Weiderpass, E. (2020). Breast Cancer. In: Anttila, S., Boffetta, P. (eds) Occupational Cancers. Springer, Cham. https://doi.org/10.1007/978-3-030-30766-0_24
Download citation
DOI: https://doi.org/10.1007/978-3-030-30766-0_24
Published:
Publisher Name: Springer, Cham
Print ISBN: 978-3-030-30765-3
Online ISBN: 978-3-030-30766-0
eBook Packages: MedicineMedicine (R0)