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Background: The emerging consensus that exposure to near-roadway traffic-related pollution causes asthma has implications for compact urban development policies designed to reduce driving and greenhouse gases.

Objectives: We estimated the current burden of childhood asthma-related disease attributable to near-roadway and regional air pollution in Los Angeles County (LAC) and the potential health impact of regional pollution reduction associated with changes in population along major traffic corridors.

Methods: The burden of asthma attributable to the dual effects of near-roadway and regional air pollution was estimated, using nitrogen dioxide and ozone as markers of urban combustion-related and secondary oxidant pollution, respectively. We also estimated the impact of alternative scenarios that assumed a 20% reduction in regional pollution in combination with a 3.6% reduction or 3.6% increase in the proportion of the total population living near major roads, a proxy for near-roadway exposure.

Results: We estimated that 27,100 cases of childhood asthma (8% of total) in LAC were at least partly attributable to pollution associated with residential location within 75 m of a major road. As a result, a substantial proportion of asthma-related morbidity is a consequence of near-roadway pollution, even if symptoms are triggered by other factors. Benefits resulting from a 20% regional pollution reduction varied markedly depending on the associated change in near-roadway proximity.

Conclusions: Our findings suggest that there are large and previously unappreciated public health consequences of air pollution in LAC and probably in other metropolitan areas with dense traffic corridors. To maximize health benefits, compact urban development strategies should be coupled with policies to reduce near-roadway pollution exposure.

Background: Prior calculations of the burden of disease from toxic exposures have not included estimates of the burden from toxic waste sites due to the absence of exposure data.

Objective: We developed a disability-adjusted life year (DALY)-based estimate of the disease burden attributable to toxic waste sites. We focused on three low- and middle-income countries (LMICs): India, Indonesia, and the Philippines.

Methods: Sites were identified through the Blacksmith Institute’s Toxic Sites Identification Program, a global effort to identify waste sites in LMICs. At least one of eight toxic chemicals was sampled in environmental media at each site, and the population at risk estimated. By combining estimates of disease incidence from these exposures with population data, we calculated the DALYs attributable to exposures at each site.

Results: We estimated that in 2010, 8,629,750 persons were at risk of exposure to industrial pollutants at 373 toxic waste sites in the three countries, and that these exposures resulted in 828,722 DALYs, with a range of 814,934–1,557,121 DALYs, depending on the weighting factor used. This disease burden is comparable to estimated burdens for outdoor air pollution (1,448,612 DALYs) and malaria (725,000 DALYs) in these countries. Lead and hexavalent chromium collectively accounted for 99.2% of the total DALYs for the chemicals evaluated.

Conclusions: Toxic waste sites are responsible for a significant burden of disease in LMICs. Although some factors, such as unidentified and unscreened sites, may cause our estimate to be an underestimate of the actual burden of disease, other factors, such as extrapolation of environmental sampling to the entire exposed population, may result in an overestimate of the burden of disease attributable to these sites. Toxic waste sites are a major, and heretofore underrecognized, global health problem.

Many interventions have been advocated to mitigate the impact of arsenic contamination of drinking water in Bangladesh. However, there are few data on the true magnitude of arsenic-related disease in Bangladesh nationally. There has also been little consideration given to possible adverse effects of such interventions, in particular, diarrheal disease. The purpose of this study was to estimate and compare the likely impacts of arsenic mitigation interventions on both arsenic-related disease and water-borne infectious disease. We found that arsenic-related disease currently results in 9,136 deaths per year and 174,174 disability-adjusted life years (DALYs; undiscounted) lost per year in those exposed to arsenic concentrations > 50 μg/L. This constitutes 0.3% of the total disease burden in Bangladesh in terms of undiscounted DALYs. We found intervention to be of overall benefit in reducing disease burden in most scenarios examined, but the concomitant increase in water-related infectious disease significantly reduced the potential benefits gained from intervention. A minimum reduction in arsenic-related DALYs of 77% was necessary before intervention achieved any reduction in net disease burden. This is assuming that interventions were provided to those exposed to > 50 μg/L and would concomitantly result in a 20% increase in water-related infectious disease in those without access to adequate sanitation. Intervention appears to be justified for those populations exposed to high levels of arsenic, but it must be based on exposure levels and on the effectiveness of interventions not only in reducing arsenic but in minimizing risk of water-related infections.

On behalf of the World Health Organization (WHO), I have undertaken a series of literature-based investigations examining the global burden of disease related to a number of environmental risk factors associated with drinking water. In this article I outline the investigation of drinking-water nitrate concentration and methemoglobinemia. The exposure assessment was based on levels of nitrate in drinking water greater than the WHO guideline value of 50 mg/L. No exposure–response relationship, however, could be identified that related drinking-water nitrate level to methemoglobinemia. Indeed, although it has previously been accepted that consumption of drinking water high in nitrates causes methemoglobinemia in infants, it appears now that nitrate may be one of a number of co-factors that play a sometimes complex role in causing the disease. I conclude that, given the apparently low incidence of possible water-related methemoglobinemia, the complex nature of the role of nitrates, and that of individual behavior, it is currently inappropriate to attempt to link illness rates with drinking-water nitrate levels.

The World Health Organization has developed standardized comparative risk assessment methods for estimating aggregate disease burdens attributable to different risk factors. These have been applied to existing and new models for a range of climate-sensitive diseases in order to estimate the effect of global climate change on current disease burdens and likely proportional changes in the future. The comparative risk assessment approach has been used to assess the health consequences of climate change worldwide, to inform decisions on mitigating greenhouse gas emissions, and in a regional assessment of the Oceania region in the Pacific Ocean to provide more location-specific information relevant to local mitigation and adaptation decisions. The approach places climate change within the same criteria for epidemiologic assessment as other health risks and accounts for the size of the burden of climate-sensitive diseases rather than just proportional change, which highlights the importance of small proportional changes in diseases such as diarrhea and malnutrition that cause a large burden. These exercises help clarify important knowledge gaps such as a relatively poor understanding of the role of nonclimatic factors (socioeconomic and other) that may modify future climatic influences and a lack of empiric evidence and methods for quantifying more complex climate–health relationships, which consequently are often excluded from consideration. These exercises highlight the need for risk assessment frameworks that make the best use of traditional epidemiologic methods and that also fully consider the specific characteristics of climate change. These include the long-term and uncertain nature of the exposure and the effects on multiple physical and biotic systems that have the potential for diverse and widespread effects, including high-impact events.

Objective: Nearly all China’s rural residents and a shrinking fraction of urban residents use solid fuels (biomass and coal) for household cooking and/or heating. Consequently, global meta-analyses of epidemiologic studies indicate that indoor air pollution from solid fuel use in China is responsible for approximately 420,000 premature deaths annually, more than the approximately 300,000 attributed to urban outdoor air pollution in the country. Our objective in this review was to help elucidate the extent of this indoor air pollution health hazard.

Data sources: We reviewed approximately 200 publications in both Chinese- and English-language journals that reported health effects, exposure characteristics, and fuel/stove intervention options.

Conclusions: Observed health effects include respiratory illnesses, lung cancer, chronic obstructive pulmonary disease, weakening of the immune system, and reduction in lung function. Arsenic poisoning and fluorosis resulting from the use of “poisonous” coal have been observed in certain regions of China. Although attempts have been made in a few studies to identify specific coal smoke constituents responsible for specific adverse health effects, the majority of indoor air measurements include those of only particulate matter, carbon monoxide, sulfur dioxide, and/or nitrogen dioxide. These measurements indicate that pollution levels in households using solid fuel generally exceed China’s indoor air quality standards. Intervention technologies ranging from simply adding a chimney to the more complex modernized bioenergy program are available, but they can be viable only with coordinated support from the government and the commercial sector.