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: 5. Persistent organic pollutants

CONCERN AND AWARENESS IS GROWING about the health effects of exposures to environmental contaminants, including those found in food. Most primary care physicians lack knowledge and training in the clinical recognition and management of the health effects of environmental exposures. We have found that the use of a simple history-taking tool — the CH²OPD² mnemonic (Community, Home, Hobbies, Occupation, Personal habits, Diet and Drugs) — can help physicians identify patients at risk of such health effects. We present an illustrative case of a mother who is concerned about eating fish and wild game because her 7-year-old son has been found to have learning difficulties and she is planning another pregnancy. Potential exposures to persistent organic pollutants (POPs) and mercury are considered. The neurodevelopmental effects of POPs on the fetus are reviewed. We provide advice to limit a patient''s exposure to these contaminants and discuss the relevance of these exposures to the learning difficulties of the 7-year-old child and to the planning of future pregnancies.CaseA 27-year-old woman who lives in a town on the shore of Lake Huron wants to have a second child but has concerns. Her 7-year-old son is being assessed by the school psychologist for a learning disorder. She tells her family physician that she saw something on television about contaminants in fish affecting children''s intelligence. She is worried that her diet may have caused her son''s learning disorder and wants advice on how to protect her second child against environmental contaminants that may cause learning problems. Her past medical history is unremarkable. She is taking no medications other than folate (0.4 mg/d). She has had only the one pregnancy. Her pregnancy and delivery of her son were uncomplicated, and the boy met the developmental milestones. The concern about a learning disorder is recent. There is no family history of congenital anomalies, early deafness or twins. Her maternal grandmother had type 2 diabetes, and her father-in-law has hypertension; the rest of the family is healthy. Because the woman is worried about environmental exposures, you take an exposure history using the CH²OPD² mnemonic (Community, Home, Hobbies, Occupation, Personal habits, Diet and Drugs)¹ to identify possible sources of environmental contaminants (Open in a separate windowThe environmental contaminants that can affect the neurobehavioural development of the fetus include metals (lead, mercury and manganese), nicotine, pesticides (e.g., organophosphates), dioxins, polychlorinated biphenyls (PCBs) and solvents (e.g., alcohol).^2,3 In this article we focus on persistent organic pollutants (POPs) and mercury. These are the contaminants identified in the environmental exposure history of the case subject (4POPs are carbon-containing chemicals that share several properties. They are lipophilic, accumulating in the fat of living organisms, and increase in quantity up the food chain. Most are semivolatile, which means that they can travel in the air thousands of miles from their source before they settle. They resist photolytic, biological and chemical degradation and persist in the environment, taking as long as a century to degrade.⁵ Twelve POPs, including 9 pesticides, have been identified by the United Nations Environment Programme as powerful threats to the health of humans and wildlife and have been targeted for elimination (6 In the 1970s many countries banned or severely restricted the use of the 9 pesticides and PCBs and implemented pollution control strategies to reduce the amount of dioxin and furan released in the environment. However, it is thought that all 9 pesticides and PCBs are still used in many countries today.Table 2Open in a separate windowDespite significant achievements in reducing the production and use of POPs, these pollutants remain ubiquitous, as evident by the global distribution of PCBs and organochlorine pesticides in butter samples from around the world.⁷ Most human exposure comes from dietary sources. POPs are ingested, stored in fatty tissue and excreted in feces and breast milk. The concentration of certain chemical contaminants in breast milk serves as an indicator of population exposure. From 1967 to 1992, there was a downward trend in the concentrations of organochlorine pesticides and PCB hydrocarbons in samples of Canadian breast milk during the phase-out of these chemicals.⁸ The estimated daily intake of PCBs from the current diet of the average Canadian is less than 1 μg/d.⁹Although everyone is exposed to a background level of POPs, certain people may have higher levels of POPs exposure because of their eating habits. Some people eat more fish than the general population. Southeast Asian Canadians, Native Americans, sport anglers and hunters who regularly eat large amounts of Great Lakes fatty fish or wildlife from the top of the food chain, such as waterfowl and waterfowl eggs, turtles and turtle eggs, muskrat, otter, moose and deer, may be at risk of high exposure.¹⁰ Northern Aboriginals, such as the Inuit of Nunavik, who consume the fat of seals and beluga and narwhal whales, have been found to have higher body burdens of POPs.^11,12     

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?     

Beyond PM2.5: The role of ultrafine particles on adverse health effects of air pollution

BackgroundAir pollution constitutes the major threat to human health, whereas their adverse impacts and underlying mechanisms of different particular matters are not clearly defined.Scope of reviewUltrafine particles (UFPs) are high related to the anthropogenic emission sources, i.e. combustion engines and power plants. Their composition, source, typical characters, oxidative effects, potential exposure routes and health risks were thoroughly reviewed.Major conclusionsUFPs play a major role in adverse impacts on human health and require further investigations in future toxicological research of air pollution.General significanceUnlike PM_2.5, UFPs may have much more impacts on human health considering loads of evidences emerging from particulate matters and nanotoxicology research fields. The knowledge of nanotoxicology contributes to the understanding of toxicity mechanisms of airborne UFPs in air pollution. This article is part of a Special Issue entitled Air Pollution, edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu.     

Ozone, air pollution, and respiratory health.

Of the outdoor air pollutants regulated by the Clean Air Act of 1970 (and recently revised in 1990), ozone has been the one pollutant most difficult to control within the federal standards. The known human health effects are all on the respiratory system. At concentrations of ozone which occur during summer air-pollution episodes in many urban metropolitan areas of the United States, a portion of the healthy population is likely to experience symptoms and reversible effects on lung function, particularly if exercising heavily outdoors. More prolonged increase in airway responsiveness and the presence of inflammatory cells and mediators in the airway lining fluid may also result from these naturally occurring exposures. Serial exposures to peak levels of ozone on several consecutive days are more characteristic of pollution episodes in the Northeast United States and may be associated with recurrent symptoms. No "high-risk" or more sensitive group has been found, in contrast to the case of sulfur dioxide, to which asthmatics are more susceptible than normals. The occurrence of multiple exposure episodes within a single year over many years in some areas of California has led to studies looking for chronic effects of ozone exposure on the lung. To date, no conclusive studies have been reported, although further work is under way. Much of what we know about the effects of this gas on the lung are based on controlled exposures to pure gas within an environmental exposure laboratory. Interactions between substances which commonly co-occur in air-pollution episodes are also under investigation.     

The health effects of particulate air pollution - a Christchurch perspective

Air quality in Christchurch has been debated widely over the last 30 years and at present there is a Draft Plan from the Canterbury Regional Council which has the main aim of improving air quality in the region. It has been shown in an inventory of emissions, that the main source of particulate pollution in the city is the use of solid fuel domestic heating appliances such as open fires and wood burners. Pollution from road traffic is considered a significant contributor to other contaminants but is less that 10% for particulate. There is local evidence that during the winter months, when atmospheric inversion conditions occur, levels of PM₁₀ (particulate matter less than 10 µm in diameter) exceed local guidelines (50 mcg m^-3 -24 hr average) approximately 30 times each year. Research performed in Christchurch suggests that these levels of air pollution account for both premature mortality and an increase in symptoms and medication requirements in susceptible sub-groups such as those with chronic obstructive airways disease. Ongoing research is planned in Christchurch and a collaborative approach between public health physicians, biostatisticians, toxicologists and clinical researchers is likely to yield further useful information which will inform the decision-making process by the Canterbury Regional Council.     

The health effects of particulate air pollution - a Christchurch perspective

Air quality in Christchurch has been debated widely over the last 30 years and at present there is a Draft Plan from the Canterbury Regional Council which has the main aim of improving air quality in the region. It has been shown in an inventory of emissions, that the main source of particulate pollution in the city is the use of solid fuel domestic heating appliances such as open fires and wood burners. Pollution from road traffic is considered a significant contributor to other contaminants but is less that 10% for particulate. There is local evidence that during the winter months, when atmospheric inversion conditions occur, levels of PM₁₀ (particulate matter less than 10 µm in diameter) exceed local guidelines (50 mcg m^-3 -24 hr average) approximately 30 times each year. Research performed in Christchurch suggests that these levels of air pollution account for both premature mortality and an increase in symptoms and medication requirements in susceptible sub-groups such as those with chronic obstructive airways disease. Ongoing research is planned in Christchurch and a collaborative approach between public health physicians, biostatisticians, toxicologists and clinical researchers is likely to yield further useful information which will inform the decision-making process by the Canterbury Regional Council.     

Respiratory health and air pollution: additive mixed model analyses

We conduct a reanalysis of data from the Utah Valley respiratory health/air pollution study of Pope and co-workers (Pope et al., 1991) using additive mixed models. A relatively recent statistical development (e.g. Wang, 1998; Verbyla et al., 1999; Lin and Zhang, 1999), the methods allow for smooth functional relationships, subject-specific effects and time series error structure. All three of these are apparent in the Utah Valley data.     

Methods for analyzing panel studies of acute health effects of air pollution

New methods are presented for analyzing repeated binary health measurements of individuals exposed to varying levels of air pollution. The methods involve a separate logistic regression of response against environmental covariates for each individual. Parameters reflecting individual susceptibility to pollutants and weather are estimated using Cox's regression techniques (1970, 1972a). The individual parameters are combined to yield summary estimates of environmental effects. The approach does not require independence of successive health measurements. It is illustrated with data on asthma and air pollution in the Los Angeles area.     

Stretching the stress boundary: Linking air pollution health effects to a neurohormonal stress response

Inhaled pollutants produce effects in virtually all organ systems in our body and have been linked to chronic diseases including hypertension, atherosclerosis, Alzheimer's and diabetes. A neurohormonal stress response (referred to here as a systemic response produced by activation of the sympathetic nervous system and hypothalamus–pituitary–adrenal (HPA)-axis) has been implicated in a variety of psychological and physical stresses, which involves immune and metabolic homeostatic mechanisms affecting all organs in the body. In this review, we provide new evidence for the involvement of this well-characterized neurohormonal stress response in mediating systemic and pulmonary effects of a prototypic air pollutant — ozone. A plethora of systemic metabolic and immune effects are induced in animals exposed to inhaled pollutants, which could result from increased circulating stress hormones. The release of adrenal-derived stress hormones in response to ozone exposure not only mediates systemic immune and metabolic responses, but by doing so, also modulates pulmonary injury and inflammation. With recurring pollutant exposures, these effects can contribute to multi-organ chronic conditions associated with air pollution. This review will cover, 1) the potential mechanisms by which air pollutants can initiate the relay of signals from respiratory tract to brain through trigeminal and vagus nerves, and activate stress responsive regions including hypothalamus; and 2) the contribution of sympathetic and HPA-axis activation in mediating systemic homeostatic metabolic and immune effects of ozone in various organs. The potential contribution of chronic environmental stress in cardiovascular, neurological, reproductive and metabolic diseases, and the knowledge gaps are also discussed. This article is part of a Special Issue entitled Air Pollution, edited by Wenjun Ding, Andrew J. Ghio and Weidong Wu.     

Abundance of siderophages in sputum: indicator of an adverse lung reaction to air pollution.

OBJECTIVE: To investigate the lung response to traffic-related air pollution by enumerating hemosiderin-laden alveolar macrophages (AM) in sputum. STUDY DESIGN: Sputum samples were collected from 103 urban adult males from Calcutta chronically exposed to automobile exhaust. Forty-nine rural individuals served as controls. AM were identified by nonspecific esterase staining. Perl's Prussian blue technique was employed for the detection of hemosiderin-laden AM (siderophages). RESULTS: The urban group, consisting of 31 traffic officers, 25 automobile service station workers and 47 street hawkers, had seven times more AM in their sputum than did the matched controls. Besides, a remarkable rise (27-fold) in the number of siderophages in sputum was observed in urban individuals. Smoking further elevated the AM count and number of siderophages. CONCLUSION: Abundant siderophages in the urban group may indicate the toxic effect of airborne pollutants on the lung, leading to phagocytosis of destroyed cells, including erythrocytes, and accumulation of iron in AM. Enumeration of siderophages in sputum appears to be a simple, noninvasive, inexpensive cytochemical technique well suited to preliminary assessment of the adverse effects of air pollution on the lungs in large, population-based studies, especially in developing countries.     

Urban air pollution: use of different mutagenicity assays to evaluate environmental genetic hazard.

The genotoxic activities associated with airborne particulate matter collected in Parma (northern Italy) have been determined. The airborne particle extracts were tested for mutagenicity using Salmonella frameshift (TA98) and base-substitution (TA100) tester strains with and without S9 microsomal activation and Saccharomyces cerevisiae strain D7 in order to determine the frequency of mitotic gene conversion and ilv1-92 mutant reversion in cells harvested at stationary and logarithmic growth phase. The relationship between mitochondrial DNA mutations and ageing, degenerative diseases and cancer prompted us to take into account the mitochondrial informational target, i.e., the respiratory-deficient (RD) mutants. The results obtained show a variability in the response for the different test systems during different months. The Salmonella mutagenicity trend was directly correlated with carbon monoxide, nitrogen oxides (NOx) and Pb concentration in airborne particulates and inversely correlated with temperature, whereas the mitochondrial genotoxic effect was higher during spring and late summer. These data suggest that the genotoxic risk assessment is a time-dependent value strictly correlated with the evaluation system being tested.     

Linking environmental and health care databases: Assessing the health effects of environmental pollutants

The assessment of pollutant effects on health status requires the mergence and analysis of two different databases: pollution measurements and health care information. This paper compares two subsets of these data: Ohio Environmental Protection Agency data on ambient air pollutants and Ohio Medicare data on respiratory diseases. Small area analysis was performed to assess statewide variations in hospital admission rates for respiratory diseases. The ambient air pollutant levels for each small area were compared to the variations in respiratory disease rates. Five groups of diseases correlated with pollutant levels. In addition, pollutant levels were significantly associated with medical complications. This study demonstrates the feasibility and benefit of linking environmental and health care databases and suggests the need for a more comprehensive, automated analysis of more pollutants and diseases.