Identifying and managing adverse environmental health effects: 3. Lead exposure

LEAD LEVELS IN NORTH AMERICAN CHILDREN AND ADULTS have declined in the past 3 decades, but lead persists in the environment in lead paint, old plumbing and contaminated soil. There are also a number of occupations and hobbies that carry a high risk of lead exposure. There is no evidence for a threshold below which lead has no adverse health effects. Blood lead levels previously considered safe are now known to cause subtle, chronic health effects. The health effects of lead exposure include developmental neurotoxicity, reproductive dysfunction and toxicity to the kidneys, blood and endocrine systems. Most lead exposures are preventable, and diagnosing lead poisoning is relatively simple compared with diagnosing health effects of exposures to other environmental toxins. Accurate assessment of lead poisoning requires specific knowledge of the sources, high-risk groups and relevant laboratory tests. In this article we review the multiple, systemic toxic effects of lead and provide current information on groups at risk, prevention, diagnosis and clinical treatment. We illustrate how the CH²OPD² mnemonic (Community, Home, Hobbies, Occupation, Personal habits, Diet and Drugs) and specific screening questions are useful tools for physicians to quickly obtain an environmental exposure history and identify patients at high risk of lead exposure. By applying effective primary prevention, case-finding and treatment interventions for lead exposure, both the individual patient and the larger community reap the benefits of better health.CaseA previously healthy 2-year-old girl and her mother visit their family physician because of the daughter''s 2-month history of intermittent complaints of a mild “tummy ache.” There is no associated vomiting, weight loss, or change in appetite, bowels or diet. There are no abnormal findings on physical examination. When asked about symptom onset the mother reports that it began shortly after the family started to renovate their kitchen. They live in an old farmhouse on the outskirts of town and drink water from a drilled well on the property. The physician decides to take an environmental exposure history using the CH²OPD² mnemonic (Community, Home, Hobbies, Occupation, Personal habits, Diet and Drugs; for children, the occupation question refers to workplace contaminants brought into the child''s environment).¹ The child''s exposure history (Open in a separate windowQuestions surrounding this case: Is the family at risk of health effects from lead exposure? Who else might be at risk? Are other laboratory tests indicated? Where can the physician get advice on the significance of the family''s blood lead levels? How should this case of lead exposure be treated?To some extent lead is one of the small success stories of environmental health. The association of lead poisoning with cognitive impairment is well established² and has resulted in the removal of lead from gasoline, paint and food cans. Despite these preventive measures, however, silent, low-level lead exposure continues to present a problem for many communities and populations. In 1997, data from the US National Health and Nutrition Examination Surveys showed that 4.4% of children in the United States had elevated blood lead levels.³ Black children living in older housing, children living in metropolitan areas with populations of 1 million or more and poor children living in older housing were at highest risk of exposure.³In Canada children living near a point-source smelter in the South Riverdale area of Toronto were tested in 1973 and found to have an unusually high mean lead level (1.34 μmol/L).⁴ Canada''s Federal–Provincial Committee on Environmental and Occupational Health suggested in 1994 that 5%–10% of Canadian children living in urban areas have blood lead levels exceeding 0.48 μmol/L, even though they are not exposed to point sources.⁵ The Ontario government estimated in 1994 that 4% of children in the province still had blood lead levels above 0.48 μmol/L;⁶ a 1992 study found that the mean level in Ontario children had fallen from 0.91 μmol/L in 1972 to 0.29 μmol/L in 1988.⁷ A study of Vancouver children using blood lead levels collected in 1989 found that 8% had elevated levels (mean 0.29 μmol/L).⁸ A later study of the children living in Trail, BC, the site of a lead and zinc smelter, demonstrated that 50% had an elevated blood lead level.⁹     

Identifying and managing adverse environmental health effects: 2. Outdoor air pollution

AIR POLLUTION CONTRIBUTES TO PREVENTABLE ILLNESS AND DEATH. Subgroups of patients who appear to be more sensitive to the effects of air pollution include young children, the elderly and people with existing chronic cardiac and respiratory disease such as chronic obstructive pulmonary disease and asthma. It is unclear whether air pollution contributes to the development of asthma, but it does trigger asthma episodes. Physicians are in a position to identify patients at particular risk of health effects from air pollution exposure and to suggest timely and appropriate actions that these patients can take to protect themselves. A simple tool that uses the CH²OPD² mnemonic (Community, Home, Hobbies, Occupation, Personal habits, Diet and Drugs) can help physicians take patients'' environmental exposure histories to assess those who may be at risk. As public health advocates, physicians contribute to the primary prevention of illness and death related to air pollution in the population. In this article we review the origins of air pollutants, the pathophysiology of health effects, the burden of illness and the clinical implications of smog exposure using the illustrative case of an adolescent patient with asthma.Case A 16-year-old girl and her mother visit their family physician in July because the daughter woke up at 6 am that morning with shortness of breath, a cough and tightness in her chest. The girl has a history of asthma and used salbutamol soon after the onset of symptoms, with some but not total relief. She reports having had no symptoms during the previous month. She had a few episodes of wheezing the previous summer, which resolved with the use of salbutamol, and a cough that persisted for 2 weeks after an upper respiratory tract infection in the winter. She has no history of allergies, hayfever or other medical problems. She is a nonsmoker and has no family history of allergies. Audible wheezing is detected on physical examination, but the girl does not appear to be in distress. Her vital signs are normal, as are the results of the ear-nose-throat and cardiovascular examinations. Respiratory examination reveals wheezing throughout chest, no focal findings and a centrally placed trachea. The girl''s calves are soft and nontender, and there is no evidence of ankle edema. Her peak expiratory flow is 240 L/min (expected for height 400 L/min). Spirometry testing is unavailable. Fifteen minutes after 2 puffs of salbutamol her peak expiratory flow increases to 320 L/min. To identify possible exposures that may have contributed to the asthma episode, the physician quickly takes an environmental exposure history using the CH²OPD² mnemonic — Community, Home, Hobbies, Occupation, Personal habits, Drugs and Diet (1Table 1Open in a separate windowQuestions surrounding this case: What was the patient''s exposure to outdoor air pollutants? How should the patient and family be counselled about dealing with these trigger factors? What are the possible inducers and triggers from indoor air pollution? How can the patient and family find out about the status of outdoor air quality in their community?     

Identifying and managing adverse environmental health effects: 1. Taking an exposure history

PUBLIC CONCERN AND AWARENESS ARE GROWING about adverse health effects of exposure to environmental contaminants. Frequently patients present to their physicians with questions or concerns about exposures to such substances as lead, air pollutants and pesticides. Most primary care physicians lack training in and knowledge of the clinical recognition, management and avoidance of such exposures. We have found that it can be helpful to use the CH²OPD² mnemonic (Community, Home, Hobbies, Occupation, Personal habits, Diet and Drugs) as a tool to identify a patient''s history of exposures to potentially toxic environmental contaminants. In this article we discuss why it is important to take a patient''s environmental exposure history, when and how to take the history, and how to interpret the findings. Possible routes of exposure and common sources of potentially toxic biological, physical and chemical substances are identified. A case of sick-building syndrome is used to illustrate the use of the mnemonic.CaseA 40-year-old married bookkeeper presents with a 3-year history of headaches. She describes having “tight,” bitemporal headaches almost daily that resolve after taking three 325-mg tablets of ASA. She also complains of a “spacey” feeling, difficulty concentrating and remembering, fatigue, a stuffy nose and a full feeling in her ears. Her symptoms improve on weekends and over the holidays and seem to be worse in the winter. Over the past 2 years she has noticed that she gets a stuffy nose and headaches when exposed to perfumes, tobacco smoke and automobile exhaust. Her past medical history is remarkable only for infantile eczema. Her family history is unremarkable other than her mother having hypothyroidism. She is taking no medications other than ASA, does not smoke, reports having no allergies and says she is happily married with no major family, financial or social concerns. She enjoys her work and coworkers. On physical examination she has puffy, dark circles under her eyes, there is loss of light reflex on her left ear drum, and her nasal mucosa appears edematous and erythematous. There are multiple excoriated, erythematous papules 5 mm in diameter on her face, anterior chest and anterior lower legs.Questions surrounding this case: What is sick-building syndrome and how do patients commonly present? What causes or contributes to sick-building syndrome? What are the risk factors? How should cases be managed?     

Removing environmental organic pollutants with bioremediation and phytoremediation

Hazardous organic pollutants represent a threat to human, animal, and environmental health. If left unmanaged, these pollutants could cause concern. Many researchers have stepped up efforts to find more sustainable and cost-effective alternatives to using hazardous chemicals and treatments to remove existing harmful pollutants. Environmental biotechnology, such as bioremediation and phytoremediation, is a promising field that utilizes natural resources including microbes and plants to eliminate toxic organic contaminants. This technology offers an attractive alternative to other conventional remediation processes because of its relatively low cost and environmentally-friendly method. This review discusses current biological technologies for the removal of organic contaminants, including chlorinated hydrocarbons, focusing on their limitation and recent efforts to correct the drawbacks.     

Linking exposure to environmental pollutants with biological effects

Exposure to ambient air pollution has been associated with cancer. Ambient air contains a complex mixture of toxics, including particulate matter (PM) and benzene. Carcinogenic effects of PM may relate both to the content of PAH and to oxidative DNA damage generated by transition metals, benzene, metabolism and inflammation. By means of personal monitoring and biomarkers of internal dose, biologically effective dose and susceptibility, it should be possible to characterize individual exposure and identify air pollution sources with relevant biological effects. In a series of studies, individual exposure to PM(2.5), nitrogen dioxide (NO(2)) and benzene has been measured in groups of 40-50 subjects. Measured biomarkers included 1-hydroxypyrene, benzene metabolites (phenylmercapturic acid (PMA) and trans-trans-muconic acid (ttMA)), 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) in urine, DNA strand breaks, base oxidation, 8-oxodG and PAH bulky adducts in lymphocytes, markers of oxidative stress in plasma and genotypes of glutathione transferases (GSTs) and NADPH:quinone reductase (NQO1). With respect to benzene, the main result indicates that DNA base oxidation is correlated with PMA excretion. With respect to exposure to PM, biomarkers of oxidative damage showed significant positive association with the individual exposure. Thus, 8-oxodG in lymphocyte DNA and markers of oxidative damage to lipids and protein in plasma associated with PM(2.5) exposure. Several types of DNA damage showed seasonal variation. PAH adduct levels, DNA strand breaks and 8-oxodG in lymphocytes increased significantly in the summer period, requiring control of confounders. Similar seasonal effects on strand breaks and expression of the relevant DNA repair genes ERCC1 and OGG1 have been reported.In the present setting, biological effects of air pollutants appear mainly related to oxidative stress via personal exposure and not to urban background levels. Future developments include personal time-resolved monitors for exposure to ultrafine PM and PM(2.5,) use of GPS, as well as genomics and proteomics based biomarkers.     

Biodegradation of toxic and environmental pollutants.

Organic chemicals that are toxic to humans and to the environment can be transformed and metabolized by a variety of microorganisms. Such chemicals include trichloroethylene, chloroform, carbon tetrachloride, toluene, phenols, chlorinated phenols, polychlorinated biphenyls and polyaromatic hydrocarbons. This review focuses on some of the most important recent developments in the biodegradation of these toxic chemicals. Depending on the compound and the organism, the extent of our understanding ranges from the molecular level to the conceptual.     

Impact of environmental pollutants on the male: effects on germ cell differentiation

A variety of so-called innocuous chemicals can have insidious and long lasting effects on the developing male reproductive system. Developmental exposures of male rabbits to common industrial contaminants in drinking water (a mixture of arsenic, chromium, lead, benzene, chloroform, phenol, and trichloroethylene); alkyl phenols (e.g. octylphenol); water disinfection by-products (e.g. dibromoacetic acid); anti-androgenic pesticides (e.g. p,p'-DDT and vinclozolin); and plasticizers (e.g. dibutyl phthalate) produce testicular dysgenesis. The lesions include testicular carcinoma in situ, also called intratubular germ cell neoplasia--the precursor lesion of germ cell tumors in men, and acrosomal dysgenesis--characterized by sharing of a dysplastic acrosome by two or more spermatids resulting in characteristic sperm acrosomal-nuclear malformations. Certain manifestations of testicular dysgenesis arch across environmental agents, and sequelae of intentional developmental exposures of rabbits duplicate what has been encountered in deer, horses, and humans for which the etiology is uncertain.     

Exposing culprit organic pollutants: a review

There is a continuing need for monitoring the health of the environment due to the presence of pollutants. Here, we review the development and attributes of biosensors by which bacteria have been genetically modified to express the luminescence genes, i.e. to glow, in a quantified manner, in response to pollutants. We have concentrated on the detection of organic hydrocarbon pollutants and discussed the molecular mechanisms by which some of these chemicals act as effector molecules on the respective regulatory systems. The future of environmental biosensors is predictably bright. As more knowledge is gathered on the sensing regulatory component, the possibility of developing targeted or pollutant-specific biosensors is promising. Moreover, the repertoire of biosensors for culprit organic pollutants is expected to be enlarged through advances in genomics technology and identification of new sensory or receptor molecules. The need for pollutant detection at concentrations in the parts per trillion range or biosensors configured in a nanoscale is anticipated.     

Vitamin A homeostasis endangered by environmental pollutants.

Normal vitamin A function depends on adequate stores of the vitamin, a finely regulated supply of the vitamin to target tissues, and an ability of cells to generate functionally active forms of the vitamin. Both endogenous and exogenous factors can adversely affect vitamin A homeostasis. Polyhalogenated aromatic hydrocarbons are ubiquitous environmental pollutants and cause severe disturbances in vitamin A metabolism, manifested by an accelerated metabolism and breakdown of vitamin A and its metabolites and a depletion of vitamin A from the body; this sequence of events accounts for the vitamin A deficiency-like symptoms associated with PHAH intoxication. The mechanism(s) responsible for these events most likely includes altered activities of enzymes that are either directly or indirectly involved in critical vitamin A metabolic pathways. Human populations that continue to be exposed to environmental pollutants, may accumulate critical levels of polyhalogenated aromatic hydrocarbons and will be at risk for inadequate vitamin A function as well as for other health impairments that have been difficult to link to any specific causes. Therefore, it is important to seriously evaluate the similarities in physiological disturbances across species that have become apparent in studies with wildlife inhabiting polluted environments similar to ours; the relevance to human health is evident.     

Histopathological effects of environmental pollutants beta-HCH and methyl mercury on reproductive organs in freshwater fish.

From various environmental pollutants studied so far, specific effects on the reproductive system of small fish species Poecilia reticulata (guppy) and Oryzias latipes (medaka) were noted in the case of beta-hexachlorocyclohexane (induction of vitellogenesis and hermaphroditism, both indicative of estrogenic activity; 32 micrograms/l) and methyl mercury (impaired spermatogenesis; 1.8 micrograms/l). The latter effect was attributed to a disturbance of mitosis.     

Persistent organic pollutants in the blood of free-ranging sea otters (Enhydra lutris ssp.) in Alaska and California

As part of tagging and ecologic research efforts in 1997 and 1998, apparently healthy sea otters of four age-sex classes in six locations in Alaska and three in California were sampled for persistent organic pollutants (POPs) and other chemicals of ecologic or environmental concern (COECs). Published techniques for the detection of POPs (specifically ∑polychlorinated biphenyls [PCBs], ∑DDTs, ∑hexachlorocyclohexanes [HCHs], ∑polycyclic aromatic hydrocarbons [PAHs], ∑chlordanes [CHLs], hexachlorobenzene [HCB], dieldrin, and mirex) in the tissue of dead otters were modified for use with serum from live sea otters. Toxic equivalencies (TEQs) were calculated for POPs with proven bioactivity. Strong location effects were seen for most POPs and COECs; sea otters in California generally showed higher mean concentrations than those in Alaska. Differences in contaminant concentrations were detected among age and sex classes, with high levels frequently observed in subadults. Very high levels of ∑DDT were detected in male sea otters in Elkhorn Slough, California, where strong freshwater outflow from agricultural areas occurs seasonally. All contaminants except mirex differed among Alaskan locations; only ∑DDT, HCB, and chlorpyrifos differed within California. High levels of ∑PCB (particularly larger, more persistent congeners) were detected at two locations in Alaska where associations between elevated PCBs and military activity have been established, while higher PCB levels were found at all three locations in California where no point source of PCBs has been identified. Although POP and COEC concentrations in blood may be less likely to reflect total body burden, concentrations in blood of healthy animals may be more biologically relevant and less influenced by state of nutrition or perimortem factors than other tissues routinely sampled.     

Solid waste treatment and disposal: effects on public health and environmental safety

The safety and acceptability of many widely used solid waste management practices are of serious concern from the public health point of view. Such concern stems from both distrust of policies and solutions proposed by all tiers of government for the management of solid waste and a perception that many solid waste management facilities use poor operating procedures. Waste management practice that currently encompasses disposal, treatment, reduction, recycling, segregation and modification has developed over the past 150 years. Before that and in numerous more recent situations, all wastes produced were handled by their producers using simple disposal methods, including terrestrial dumping, dumping into both fresh and marine waters and uncontrolled burning. In spite of ever-increasing industrialisation and urbanisation, the dumping of solid waste, particularly in landfills, remains a prominent means of disposal and implied treatment. Major developments have occurred with respect to landfill technology and in the legislative control of the categories of wastes that can be subject to disposal by landfilling. Even so, many landfills remain primitive in their operation. Alternative treatment technologies for solid waste management include incineration with heat recovery and waste gas cleaning and accelerated composting, but both of these technologies are subject to criticism either by environmentalists on the grounds of possible hazardous emissions, failure to eliminate pathogenic agents or failure to immobilise heavy metals, or by landfill operators and contractors on the basis of waste management economics, while key questions concerning the effects of the various practices on public health and environmental safety remain unanswered. The probable and relative effects on both public health and environmental safety of tradition and modern landfill technologies will be evaluated with respect to proposed alternative treatment technologies.     

Human cancer from environmental pollutants: the epidemiological evidence

An increased risk of mesothelioma has been reported among individuals experiencing residential exposure to asbestos, while results for lung cancer are less consistent. Several studies have reported an increased risk of lung cancer risk from outdoor air pollution: on the basis of the results of the largest study, the proportion of lung cancers attributable to urban air pollution in Europe can be as high as 10.7%. A causal association has been established between second-hand tobacco smoking and lung cancer, which may be responsible for 1.6% of lung cancers. Radon is another carcinogen present in indoor air, which may be responsible for 4.5% of lung cancers. An increased risk of bladder might be due to water chlorination by-products. The available evidence on cancer risk following exposure to other environmental pollutants, including, pesticides, dioxins and electro-magnetic fields, is inconclusive.