Keywords

7.1 Introduction

Building materials can act as a source of pollutant emission and thereby affect the quality of indoor air (US EPA 1994). The number of compounds emitted from building materials varies. Exposure to these compounds can be hazardous to human health. There have been several struggles and efforts to limit the exposure in the building design industry. The idea is that if in a building design, a building material is known to be a source of pollution and needs more ventilation to neutralize its effects, it will be more advisable to use an alternative material that has less emission rate (CIBSE 1996).

Heavy metals pose a high risk of adverse effects on human health, some metals are carcinogenic, neurotoxic and immunotoxic. Metals are usually found in the environment and as a result of the extensive use in the environment, human exposure is unavoidable. Understanding the mechanisms of heavy metal toxicity has been challenging as a result of the association between metals and living systems. Research has shown that metals are compromised in cardio-respiratory related illnesses that are linked to the pollution of the air (Burnett et al. 2000; Vincent et al. 2001; Claiborne et al. 2002; Sorensen et al. 2005). Osornio-Vargas et al. (2003) reported that transition metals are linked to oxidative stress and respiratory dysfunction.

Some metals are indispensable and vital for life as a result of their role in the provision of required enzymes but excessive concentration of these enzymes can be harmful either by choking important functional groups or altering the conformation of protein molecules (Collins and Stotzky 1989). Metals have a profound effect on physiological and biochemical processes which include photosynthesis and respiration inhibition (Vangronsveld and Clijsters 1994). Transition elements are used in making paints and this poses a serious threat to human health as a result of deviation from manufacturer’s standard, unsuitable storage, carelessness in handling and transportation. Lead based paint is still being used in a lot of homes today. The peeling and damage of lead-based paint is hazardous and it can amount to threat to human health especially in children. Cadmium, mercury and some heavy metals are naturally occurring but human exposure occurs as a result of anthropogenic activities.

This chapter focuses on the heavy metals which include lead, cadmium, chromium and mercury as it relates to building materials with emphasis on their structure, uses and its toxicological effects. Awareness about environmental pollutants and their adverse effects on human health cannot be over-emphasized as the aim is to protect people from avoidable exposures.

7.2 Lead

Lead metals play an important role in transporting water and its usage can be traced back as far as the Roman times. Roofing materials can also be produced from lead metals. Lead metals decay slowly which justify its high acceptability in usage. However, lead has been known to be toxic; the first reported effect of lead on human health was the fall of Roman Empire which was influenced by lead poisoning (Dutrizac et al. 1982; Hodge 1981; Nriagu 1983). In the home today, health problems from lead can be from lead pipes which are used in connecting homes to the water source; it can also be from lead roofing and guttering; it can also be from lead-based house paint (Wani et al. 2015). Lead absorption in the body accumulates in the blood, bones, liver, kidney, brain and skin. Krzywy et al. (2010) revealed that lead causes reproductive dysfunction, hepatic dysfunction and also affects the immune and gastrointestinal systems (Krzywy et al. 2010).

7.2.1 Lead Piping and Water Contamination

Lead pipes are used to convey water from the water main source to the apartment buildings. Lead pipes are buried inside the soil thereby making it difficult to establish their presence or absence. In the 1800s, the beginning of urbanization and mass housing brought about the use of lead connection pipes. Despite the caution that was expressed about the use of lead pipes in the nineteen century (Troesken 2006), the use of lead pipes continued till the 1980s in both Europe and North America. The occurrence of lead pipes in different countries in Europe is shown in Table 7.1. The length of the pipe varies from a few meters to hundreds of meters depending on the distance between the dwelling and the water source. The risk is associated with the length of the pipe, the longer the lead pipe, the greater the risk to human well-being.

Table 7.1 Lead pipes occurrence in Europe (Adapted after: Van den Hoven et al. 1999)
Full size table

Hayes and Skubala (2009) reported that about 25% of dwellings in Europe are likely to be supplied with drinking water through lead pipes. About 2–3% of dwellings in the US and Canada use lead pipes (IWA 2010). The corrosion of the pipe and the contact of the water with the lead pipe determine the amount of lead that will be present in the drinking water. Lead concentration in drinking water can vary from <1 to hundred µg/l.

7.2.2 Lead Toxicity

Lead is stored in the liver and also can be found in the kidneys. Its distribution can also be in the brain, adrenals, prostate, ovary, spleen, fat tissues, heart and spinal cord (Seervarisai et al. 2015). Lead is harmful to human health; reports from clinical researches have confirmed this claim (Lanphear et al. 2000; Menke et al. 2006; Jusko et al. 2008; Khalil et al. 2009). Lead affects many biochemical processes such as calcium inhibition and reaction with proteins. Upon absorption, lead substitutes with calcium and this leads to interaction with biological processes and thereby causing abnormalities. As a result of its reaction with protein, Pb causes changes in enzyme structure and causes dysfunction in the binding site. The primary mechanism that leads to lead toxicity is the oxidative stress that is caused by lead.

Research from the World Health Organization has shown that lead affects children’s central nervous system and development (WHO 2016). Children less than six (6) years old are very susceptible to the harmful effect of lead because of the brain growth and development (Wani et al. 2015; WHO 2016). Lead can impair memory, lower intelligent quotient (IQ) in children. Reports have shown that lead has profound effects on speech, hearing, vomiting and intestinal pain. At high concentration as shown in Table 7.2, lead poisoning can cause anemia, paralysis, convulsion or death (Giel-Pietraszuk et al. 2012; Rehman et al. 2018). During pregnancy, maternal lead exposure can be transferred to the developing embryo via placenta (Rehman et al. 2018; Omeljaniuk et al. 2018). In addition, during pregnancy, when the calcium intake of the mother is low, the lead that is stored in the mother’s bone can be transferred via the blood to the fetus. This confirms that maternal exposure to lead before or during pregnancy can have a devastating effect on the developing embryo as a consequence of the stored lead in the bone (CDC 2010; Bellinger 2013). As a result of the toxicity of lead in children, WHO has recommended blood lead concentration of 5 µg/dL or less for children (CDC 2010; Wani et al. 2015; WHO 2016).

Table 7.2 Level of blood lead and degree of lead poisoning and the symptoms in children and adult (Adapted after: Giel-Pietraszuk et al. 2012)
Full size table

Lead also has harmful effects in adults. It can lead to dysfunction in the nervous system (fatigue, drowsiness), circulatory system (increased blood pressure), hormones (fertility abnormalities, decreased libido), cardiovascular system and it can also lead to death (Wani et al. 2015). Individuals with high concentration of lead in their blood (500–870 µg/L) often encounter sinus node dysfunction and also atrioventricular block (Zawadzki et al. 2006). In adults, lead concentration in the blood has been linked to blood pressure. Nevertheless, its effect on blood pressure depends on dosage and exposure time (Wani et al. 2015). Navas-Acien and colleagues confirmed that exposure to lead is linked to hypertension (Navas-Acien et al. 2007). Research has also revealed the relationship between blood lead concentration and cancer especially brain, lung tumor (Steenland et al. 2019).

7.2.3 Replacement of Lead Pipes

There are some speculations that lead pipes have been withdrawn but of a truth, very few have been removed and many are still been used especially in places like Africa. Some water corporations also claim that lead pipes has been removed but this has been less effective because some homes still use lead pipes within their dwellings (DWI 2010). Efforts have been made to remove all lead pipes but internal lead piping has been the challenge as a result of the stress and the cost involved. Considering the various harmful effects of lead on children and adults, the idea is to have a lead pipe-free home. To achieve this, laws should be made that the home-owners should remove all the lead pipes before sale or letting it out. In the meantime, Hayes and Croft suggested that the application of point-of-use filters can be used to remove lead from water (Hayes and Croft 2012). Leaded solder was allowed in the 1980s. Many homes still have a leaded solder and the removal is not realistic, unless under special conditions. This suggests that water supply systems require a strategy to control corrosion so as to minimize these lethal effects. In addition, lead-free brass with about 8% lead has been allowed. However, in the 1980s, brass fittings containing >8% lead were used and many homes still have this internal pipework system. To have effective control, all countries need to take after the US by enforcing the use of brass with <0.25% of lead and ban the use of leaded solder.

7.3 Cadmium

7.3.1 Cadmium History and Application

Cadmium (Cd) was first discovered in Germany by Friedrich Stromeyer in 1817. Cd is readily found in little concentration mostly alongside sulphide of zinc, lead and copper. Associated use of Cd as building materials include pigments, stabilizers of PVC and alloys, protective agents of steel from corrosion, Ni–Cd batteries (WHO 1992; IARC 1993; Hayat et al. 2019). Cd compounds are used as coloring agents in borosilicate glass. Cd is a rare element; its estimation is around 0.1–0.2 ppm which signifies that it is the 67th element in order of abundance (Brewers et al. 1987).

7.3.2 Chemical Forms and Properties of Cd

Cadmium (Cd) is a member of the group XII in the periodic table of chemical elements. Cd atomic mass is as a result of eight stable isotopes. The colour of Cd is silvery-white. Cd properties are synthetically related to zinc and mercury. In the s orbital it has double electrons and a complete d orbital. Cd is resistant to corrosion hence, the main reason it serves as a protective agent. It is insoluble in water; it forms cadmium oxide when burned in air.

7.3.3 Cadmium Toxicity

The US environmental protection agency identifies cadmium as one of the 126 priority pollutants. Cadmium is absorbed in high quantities from air, food and water contaminations which confirms the role that building materials play in its absorption. Cadmium has the potential to accumulate throughout a lifetime which makes it more harmful. Cadmium salts accumulate and lead to the toxicity of many organs which includes the kidney, lungs, brain, testes, and the heart. Cadmium can cause anemia, kidney failure, anosmia, non-hypertrophic emphysema. People that make cadmium products like batteries, plastic, soldering or welding building materials can be exposed to cadmium.

Cadmium inhalation linked with respiratory diseases which include lung cancer. Mona and colleagues revealed an increase in cadmium level of smoker’s urine (Mona et al. 2018). In addition, it was reported that the percentage of bone pain of smokers increased (95%) non-smokers (37.7%). This suggests that exposure to cadmium results in an ototoxic effect which can in turn lead to bone tissue loss. The epidemic of Itai-Itai disease was as a result of cadmium exposure (Hagino and Yoshioka 1960).

Cadmium exposure even at low doses can result in abnormalities in male and female reproduction and thereby affect pregnancy and offspring outcomes (Kumar and Sharma 2019). Exposure to cadmium also causes irregularities in the menstrual cycle, alterations in reproductive hormones, pregnancy loss, premature birth and reduction in birth weight (Lokhande et al. 2004). Cadmium is also known to be an endocrine disruptor because it interferes with many hormonal signaling pathways, one of such is that it can bind estrogen receptor α; it can also interfere with signaling transduction through estrogen and mitogen-activated protein kinase (MAPK) signaling pathways (Söderholm et al. 2020).

Cadmium exposure has an epigenetic effect and can also alter gene expression. Exposure to cadmium can result in DNA methylation and histone modifications. Heavy metals can utilize their toxicity through the miRNA. Endogenous miRNA alterations have been associated with impaired signaling pathways which subsequently result in different kinds of cancer and disorders (Wallace et al. 2020). Takiguchi and colleagues (2003) in their study reported that short time exposure (24 h–1 week) results in hypomethylation, whereas long exposure (8–10 weeks) leads to hypermethylation (Takiguchi et al. 2003).

Cadmium has been classified as a cancer causing agent (WHO 1992; IARC 1993). Cadmium toxicity results in oxidative stress that further promotes the spread of tumor through its effect on cell cycle (Rani et al. 2014). Cadmium inhibits DNA repair mechanisms and this can lead to accumulation of damaged DNA hence the initiation of cancer (Giaginis et al. 2006). A study conducted from 2006 to 2014 as reported by Nawrot and colleagues showed that lung cancer is linked to the exposure to cadmium. In this study, it was revealed that cadmium is a risk factor for lung cancer (Nawrot et al. 2015). Furthermore, scientific data also suggests that cadmium exposure can be associated with prostate cancer (Julin et al. 2012), urinary bladder cancer (Feki-Tounsi and Hamza-Chaffai 2014), cancer of the kidney (Song et al. 2015) and pancreas cancer (Chen et al. 2015).

Studies in animal models have shown that antioxidants (vitamin C and E) can protect from toxicity induced by cadmium (Ognjanovic et al. 2003; Beytut et al. 2003). Membrane separation and reverse osmosis are sometimes used to get rid of heavy metals in liquid but it is very expensive and requires large quantities of chemicals.

7.3.4 Biomonitoring of Cadmium

Biomonitoring studies involving cadmium level helps physicians and public health officials to ascertain exposure level of cadmium in individuals and groups of population. Cadmium level in urine and blood help in biological monitoring of cadmium. Blood cadmium usually reveals current exposure and it ranges from 0.2 to 0.8 pg/l. Although, smokers are known to have higher concentrations ranging from 1.4 to 4.5 pg/l as reported by Elinder et al. (1994). Urinary excretion of cadmium for a day is a biological marker of lifespan exposure, whereas cadmium concentration in blood reveals current exposure (Staessen et al. 1996). Data from biomonitoring studies can help researchers to conduct future research on exposure and health effects of cadmium.

7.4 Chromium

7.4.1 Chromium History and Application

Chromium is commonly used together with other metals. It was discovered by Louis Vauquelin in 1797. Louis Vauquelin discovered chromium while he was making an experiment with a material called ‘Siberian red lead’, which is also known as ‘mineral crocoite (PbCrO4)’. Vauquelin produced chromium oxide (CrO3) by putting together crocoite and hydrochloric acid (HCl) Application of chromium as building materials include dyes and paints, stainless steel, chrome plating and metallurgy.

Chromium is being added to metals to make stainless steel. Its corrosion resistant nature extends the lifespan of products making it an important ingredient in building materials. About 80% of mined chromium is used for metallurgical processes, in which many of the0se are used in making stainless steel. About 15% is used in the manufacturing of chromium chemicals and about 5% is used in refractory applications. The corrosion resistant nature and the attractive nature form the major factor for its selection. Potassium dichromate (K2Cr2O7) is used in chemicals for leather tanning and also used for wood preservation (Johnson et al. 2006). Copper chrome arsenic (CCA) is used in the preservation of woods and it contains chromium trioxide, arsenic pentoxide and copper (II) oxide. It is made available in form of paste or water-based concentration and CCA has been used for preservation of wood so as to prevent decay caused by fungi and wood-boring insects (Cocker et al. 2006). Lead Chromate (PbCrO4) has also been known to be used as yellow pigments in paints.

7.4.2 Chemical Form and Properties of Chromium

Chromium is used in manufacturing stainless steel and pressure-treated wood. Data from exposure to chromium from occupation shows that about half a million workers are exposed to chromium in the US and unspecified millions globally (Zhitkovich 2002; OSHA 2006). Exposure to chromium occurs through air emissions (cigarette smoke, industrial, automobile smoke) and water contamination (industrial release, wastewater leaching) (Welling et al. 2015). Cr(0) usually occurs in alloys with metals such as iron in its metallic form. Through welding, Cr(0)is converted to chromium (III) and chromium (VI). Chromium (III) is an indispensable micronutrient that is required in metabolism of glucose (Schwarz and Mertz 1959), but in the present-day, the report is now being debated (Ali et al. 2011; Xia et al. 2016; Vincent 2017, 2019).

Employees are exposed to chromium in more than 80 different industries. In construction companies, tanning, electroplating, metal finishing, welding, wood preservatives and pigments production, workers are exposed to chromium (IARC 1990).

7.4.3 Chromium Toxicity

Regardless of the mode of chromium absorption, the adverse health effects caused by chromium usually depend on the oxidation state, chemical species bioavailability and solubility. After absorption, chromium compounds can undergo alkylation and oxidation state alteration.

Chromium (III) has low membrane permeability, and this can lead to change in the membrane morphology, disruption in cell functions and also can induce DNA damage (Fang et al. 2014). Transferrin, a β-globulin, helps to protect against chromium toxicity that is obtained from food consumption by inhibiting the aggregation of chromium (III) and mediating chromium (III) transmembrane transportation. The transferrin (Tf) gene is distinct having about 38 recognized variants, studies linking the recognized variants of transferrin to Cr (III) transport is required to elucidate the effects of the variant (Edward et al. 2019).

Chromium (VI) exposure may affect many systems in the body which include skin, irritation in respiration, kidney failure, hepatic (liver damage and increase in liver enzymes), genetic (genotoxicity, mutagenicity and carcinogenicity) and reproductive effects (birth weight, anovulation, irregular menstrual cycle) (IARC 1990; Teklay 2016; Wang et al. 2017). However, the gravity of these health effects depends on the extent of the exposure to chromium (VI).

Chromium (VI) compounds have been identified as the primary source of lung cancer (IARC 1990). Chromium (IV) has been considered to be carcinogenic (IARC 1990). Low concentration of Chromium (VI) causes DNA breakage. The established limit by the Occupational Safety and Health Administration (OSHA 2006) was 5 µg m−3, recent risk assessment has revealed that of 1000 employees cancer deaths, about 10–50 were exposed to this limit (Beyersmann and Hartwig 2008). Deposits of chromium (VI) are shown in different studies to cause tissue damage which eventually leads to lung cancer. Accumulation of Cr (VI) in tissues leads to DNA impairment, tumor initiation which eventually causes carcinogenesis (Ishikawa et al. 1994; Proctor et al. 2014; Browning and Wise 2017).

In vitro studies showed that chromium (VI) can form a reaction with histone and then be transported to the nucleus (Levina et al. 2006). The reaction and transportation suggests a mechanism of DNA damage. Cr (VI) exposure induces histone modifications which include reduced acetylation and increased biotinylation and this mechanism has been suggested as a mechanism of tumor initiation and progression (Xia et al. 2014).

Cr (VI) compounds are soluble penetrating the cell through a negatively charged ion carrier (Buttner and Beyersmann 1985). On getting to the cell, reduction reaction takes place by various chemical and enzymatic reductants and it eventually forms Cr (III). There is formation of reactive chromium species Cr (II), Cr (IV), Cr (V) during this reduction reaction. This can induce reactive oxidative stress (ROS) (Borthiry et al. 2007).

7.4.4 Biomonitoring of Chromium

The literature has provided enough reports as regards the biomonitoring of chromium level in urine in exposed populations. For instance in population of people working with materials linked to chromium (for instance, welder) (Mutti et al. 1984; Minoia and Cavalieri 1988; Brand et al. 2010). Little has been done regarding investigating residential populations that are potentially exposed to environmental chromium, the reason being the presence of high levels of chromium in urine of both exposed and controlled populations.

In a population of people handling timber treated with copper chrome arsenic (CCA), exposure was confirmed (Garrod et al. 1999). Dermal exposure was the primary route of exposure and exposure through inhalation was observed as relatively low. Chromium concentration in urine of workers that were exposed to wood preservatives is significantly higher than the non-exposed people.

Human biomonitoring results and concentration of metal air of 36 welders welding solid steel were revealed by Mutti et al. (1984). It was revealed in this study that water soluble Cr (IV) concentrations in the air ranged from 0.010 to 0.152 mg m−3 with a median of 0.065 mg m−3, while total Cr concentrations in the air ranged from 0.012–0.224 mg m−3 with a median of 0.094 mg m−3. The mean urinary chromium was 33.3 µg/g. Gube and colleagues revealed that after exposure, the mean chromium concentration in the urine is 1.61 µg/l (Gube et al. 2013).

7.5 Mercury

7.5.1 Mercury History and Application

Mercury is represented by the symbol “Hg”. “Hg” was coined from Latin word “hydrargyrum”. Mercury is liquid at ambient temperature. The use of mercury as building materials is related to its use in fluorescent lamps. It can also be utilized in technological applications such as thermometers, barometers, and gas meters. Culturally, it can be used as preservatives in home paints and also as antiseptics. The technological and cultural uses of mercury make it an indoor air pollutant in residential places.

Properties such as low melting and boiling points, biological cycle’s participation makes mercury (Hg) to be considered as global pollutants. Mercury is released through natural and anthropogenic activities but studies have revealed that it is the anthropogenic emission that contaminates the environment. Estimates revealed that total release of mercury from both sources from past activities is 6000–11000 tons per year (Swartzendruber 2012). It is believed that emission through anthropogenic activities constitute about 80% of the yearly discharge to the environment. Following the industrial revolution, the mercury level of the surface water has tripled. Mercury concentrations are now about 10–12 times higher in marine animals today as compared to the preindustrial times (prior to 1800) (Braune et al. 2005; Lamborg et al. 2014). Mercury compounds are mostly used in paint production. The content of mercury in a commercial paint is usually about 0.05% and this may cause air pollution.

7.5.2 Chemical Form and Properties of Mercury

Mercury is an odorless and silvery metallic liquid and it is insoluble in water. It is the 80th member on the periodic table. Mercury is ubiquitous and it is usually in three forms; (1) elemental (2) inorganic and (3) organic mercury. Reports have shown that all the forms of mercury have toxic effects on mammals (Clarkson et al. 2003; WHO 2007). Elemental (metallic) Hgwhich is liquid at room temperature has a high vapour pressure and it is released to the environment in the form of mercury vapour. The methylation of the inorganic form of mercury leads to the formation of the methylmercury. In the environment today, mammalian species are exposed to all the three forms of mercury; elemental (Hg), inorganic [Hg(I)], [Hg(II)] and organic mercuric compounds (WHO 2007).

Human exposure to elemental mercury is from artisanal gold mining. Inhalation of vapourized elemental mercury is usually absorbed into the blood and crosses the blood-brain barrier. Estimation shows that 10–15 million miners (mostly in developing countries) are affected by chronic mercury intoxication (Ha et al. 2017).

7.5.3 Mercurial Toxicity

Generally, mercury(II) chloride or mercuric chloride (HgCl2) and methylmercury (MeHg) play a crucial role in inducing many biological processes ranging from increased lipid peroxidation to formation of ROS, depletion of glutathione (GSH) (Berntsen et al. 2003; Crespo-Lopez et al. 2009). Additionally, exposure to HgCl2 and MeHg alters cell signaling (Chen et al. 2006), reduced integrity of cell membrane (Polunas et al. 2011), impaired DNA repair mechanism (Christie et al. 1985; Gadhia et al. 2012; Pieper et al. 2014; Ryu et al. 2014), immunomodulatory impacts (Gallagher et al. 2011) and also altered the DNA methylation (Farina et al. 2011) eventually resulting in adverse health effects. Many literature reviews discuss various mechanisms by which mercury exposure results in neurotoxicity and cell damage (Clarkson 2002; Mergler et al. 2007; Crespo-Lopez et al. 2009; Farina et al. 2011; Antunes et al. 2016).

In vitro studies have revealed the relationship between MeHg intoxication and neuronal deaths. Exposure to MeHg results in neuritic degeneration (Fujimura et al. 2009), oxidative damage (Yin et al. 2007) and this disruption of biological processes leads to neuronal deaths. It has also been well-documented that organic mercury has the ability to bind with thiol residues which eventually lead to dysfunction in protein containing thiol groups. Mercury exposure can also inhibit the activities of enzymes that correct oxidative stress in cells. MeHg and HgCl2 inhibit the action of thioredoxin (Trx), glutathione reductase (GR) thioredoxin reductase (TrxR), superoxide dismutase (SOD), while MeHg inhibit the action of glutaredoxin (Grx), glutathione peroxidase (Gpx), neuronal nitric oxide synthase (nNOS) (Carvalho et al. 2008; Farina et al. 2009; Carvalho et al. 2011; Robitaille et al. 2016).

In vivo studies revealed that methylmercury is neurotoxic and teratogenic (Stern et al. 2004; Karagas et al. 2012). Toxicogenomics and proteomics studies of tissues from whole organisms revealed that exposure to organic and inorganic mercury can change gene expression and proteins that are involved in oxidants and antioxidants defenses. Altered antioxidants enzymes include glutaredoxin (Grx), glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), thioredoxin (Trx), thioredoxin reductase (TrxR), nitric oxide synthase (NOS), peroxiredoxin. Metallothioneins (MTs), genes and proteins involved in metabolism were altered in unicellular alga Chlamydomonas Reinhardtii (Beauvais-Flickr et al. 2017), yeast (Jin et al. 2008), macrophytes (Dranguet et al. 2017), Caenorhabditis Elegans (Ruda Galvyte et al. 2013), Zebra (Ho et al. 2013), pregnant mice (Robinson et al. 2010; Godefroy et al. 2012) and human (Pinheiro et al. 2008; Grotto et al. 2010).

7.5.4 Biomonitoring of Mercury

Excretion of mercury occurs within a week after exposure. It can be found in urine and faeces at low levels after some months (Goldfrank et al. 1994). Mercury levels in blood that are higher than 35 µg/dl and mercury levels in urine that are higher than 150 µg/dl are considered toxic to humans (NPIS 1996). Mercury vapour in air should not exceed 0.1 mg/m3. A report showed that 200 mg/l of mercury in blood and 50 mg/g in hair are the established limits and a higher concentration is considered toxicity (Harada et al. 1997).

For biological monitoring of mercury exposure, the common biological samples to examine mercury exposure due to occupation are urine and blood. Hair is best known to examine environmental exposure to methylmercury (Satoh 2000). The mean urinary concentration of mercury in the US population is 0.72 µg/l (95% CI, 0.6–0.8), the mean blood concentration is 0.34 µg/l (95% CI, 0.3–0.4) (CDC 2003). Brune and colleagues (1993) reported that in Europe, the blood concentration is higher. Also, exhaled air could be a possible biomarker of exposure to elemental mercury vapour as a result of its excretion through the lungs. The assessment of methylmercury is done through the blood and scalp hair.

7.6 Remedial Actions

Reduction in metal emissions from industries and waste incinerators will help to reduce environmental and human exposure. Older fluorescent bulbs should be changed to the new energy-efficient bulbs, because the older ones contain mercury. In schools, especially in chemistry laboratories, mercury may be present or in health clinics generally where thermometers and thermostats are often used, it should be handled by experts and also with care. Planting of trees and other vegetation should be encouraged in urban areas so as to improve the quality of life. Trees help in particle uptake and hence can be helpful in lessening the toxicity of heavy metals.

7.7 Recommendations

7.7.1 New Buildings

  1. 1.

    Avoid the use of lead piping

  2. 2.

    Avoid connection of new pipeline to an old lead connection pipe

  3. 3.

    Avoid the use of soldiers containing lead

  4. 4.

    Should in case brass fittings are used, ensure that the lead content is less than 0.25%

  5. 5.

    Avoid inhaling dust and smokes (cigarette or automobile)

  6. 6.

    Parents and guardians should monitor infants and toddler and prevent them from ingesting dust from soil through hand-mouth activities.

7.7.2 Old Building

  1. 1.

    In the presence of lead pipes or brass containing high contents of lead, in the morning before taking a drinking water from the pipe, flush the pipework for at least 2 min.

  2. 2.

    Lead pipes or fittings that contain high lead contents should be removed and treated as hazardous waste.