Publications by authors named "J K Chandalia"

Objective: US Environmental Protection Agency (EPA) based its benzene carcinogenicity assessment on the Pliofilm cohort. We evaluated associations between benzene exposure and acute nonlymphocytic leukemia (ANLL) and acute myelocytic leukemia (AML) risks using this cohort's updated exposure estimates and mortality data.

Methods: We calculated standardized mortality ratios (SMRs) for ANLL/AML using lifetable analyses, with various exposure quantile categories and lag times.

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A pooled-analysis by Lanphear et al. (2005) of seven cohort studies of the association between blood lead (BPb) concentrations in children and measures of their intelligence concluded that "environmental lead exposure in children who have maximal blood lead levels <7.5 μg/dL is associated with intellectual deficits.

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The US EPA is evaluating controlled human ozone exposure studies to determine the adequacy of the current ozone National Ambient Air Quality Standard of 75 ppb. These studies have shown that ozone exposures of 80 ppb and greater are associated with lung function decrements. Here, we critically review studies with exposures below 80 ppb to determine the lowest ozone concentration at which decrements are causally associated with ozone exposure and could be considered adverse using the Adverse Effects/Causation Framework.

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Both classical and Berkson exposure measurement errors as encountered in environmental epidemiology data can result in biases in fitted exposure-response relationships that are large enough to affect the interpretation and use of the apparent exposure-response shapes in risk assessment applications. A variety of sources of potential measurement error exist in the process of estimating individual exposures to environmental contaminants, and the authors review the evaluation in the literature of the magnitudes and patterns of exposure measurement errors that prevail in actual practice. It is well known among statisticians that random errors in the values of independent variables (such as exposure in exposure-response curves) may tend to bias regression results.

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The effects of 0.1 to 0.6 ppm nitrogen dioxide (NO2) on airway hyper-responsiveness (AHR) to airway challenges in asthmatics have been evaluated in several controlled exposure studies.

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