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Biomedical subjects

P Flessel

Publications and source records attributed to P Flessel.

8 recordsLinked to original sources
PubMed1997

Biological monitoring for mercury within a community with soil and fish contamination.

To assess the impact of elevated levels of inorganic mercury in soil and dust and organic mercury in fish, biological monitoring was conducted among Native Americans living next to an inactive mercury mine in Clear Lake, California. Of resident tribal members, 46% (n = 56) participated in biomonitoring. Urine mercury levels are equivalent to background, indicating that soil and dust exposures among study participants are not substantial. The average blood organic mercury level among study participants is 15.6 +/- 8.8 micrograms/l (n = 44), which is higher than levels reported by others among those who do not consume fish (2 micrograms/l). Consistent with results from other studies, a correlation between fish consumption and blood organic mercury is observed (p = 0.03). The margin between observed and established adverse effect levels for adults is examined for blood organic mercury and found to be less than 10-fold for 20% of the study population. Protective public health efforts for the study population and other similarly exposed populations, notably those who consume commercial fish products, are considered.

Adult↗
PubMed1996

Evaluation of lead levels in children living near a Los Angeles county battery recycling facility.

This cross-sectional study examined the association between environmental lead measurements surrounding a Los Angeles County battery recycling facility and the blood lead levels of the children living nearby. Environmental lead measurements and blood lead levels of young children living in a community adjacent to a stationary lead source were compared to those living in a community without a stationary lead source. Predictors of blood lead level were identified. The blood lead levels of the children living near the secondary lead smelter were within the normal range (< 5 micrograms/dl). The absence of ground cover was associated with slightly increased blood lead levels; however, this increase was not of biological significance. Lead levels in surface soil near the stationary lead source were elevated compared to the control community; however, the soil affected community, which may be due in part to controls recently installed at the stationary lead source.

California↗
PubMed1995

Lead levels in the household environment of children in three high-risk communities in California.

To assess environmental lead contamination in the household environment of children in high-risk areas of California, three urban locations were surveyed by the California Department of Health Services. Plant, soil, and dust lead levels were measured and a questionnaire was administered. This survey estimates that 3 million homes in California (27%) may have exterior paint lead levels > or = 5000 ppm, and 1.3 million homes (12%) may have interior paint lead levels > or = 5000 ppm. The highest concentrations of lead in paint were found on exterior surfaces and, for homes built between 1920 and 1959, on trim. Age of housing was the best predictor of lead in soil and dust; homes built before 1920 were 10 times more likely to have soil lead levels > or = 500 ppm compared to post-1950 homes. Most of the variability in dust lead levels could not be explained by factors measured in this survey. Sources of lead in the home were more highly correlated with lead dust concentration levels than they were with lead dust loading levels. Households with members reporting a lead job were twice as likely to have high dust lead levels compared to households with no one reporting a lead job. The significant differences in dust lead concentration levels between communities were not reflected in differences in dust lead loading levels. Measuring dust lead loading levels does not appear to be a meaningful sampling method for risk assessment in the context of prioritizing abatement.

California↗
PubMed1993

Genetic toxicity of malathion: a review.

Mammalian in vivo and in vitro studies of technical or commercial grade malathion and its metabolite malaoxon show a pattern of induction of chromosome damage, as measured by chromosome aberrations, sister chromatid exchanges, and micronuclei. Experiments with purified (> 99%) malathion gave weak or negative results. In contrast to the cytogenetic effects of technical grade malathion, responses in gene mutation assays were generally negative except for malaoxon, which was positive for mammalian gene mutations in both tested instances. This result also could be a consequence of chromosome level changes, however. Dermal exposure, a common human route, caused cytogenetic damage in test animals at doses near those producing positive results by intraperitoneal injection. Workers who apply technical grade malathion and other pesticides have higher levels of chromosomal damage than unexposed individuals. Because of the inactivity of malathion mixtures in gene mutation assays, malathion has been thought to be of little genotoxic concern. However, the pattern of chromosome damage in animals and mammalian cells in culture (including human) indicates that technical grade malathion and its components have not been adequately studied for genotoxic potential in humans.

Animals↗
PubMed1991

Seasonal variations and trends in concentrations of filter-collected polycyclic aromatic hydrocarbons (PAH) and mutagenic activity in the San Francisco Bay area.

Air monitoring in the San Francisco Bay Area was carried out to measure outdoor community air concentrations of polycyclic aromatic hydrocarbons (PAH) and mutagenic activity (mutagenicity) in particulate organic matter (POM). Monitoring began in 1979 and is currently conducted at six stations. PAH and mutagenicity tests were performed on organic extracts prepared from high volume (hi-vol) filters composited every four months, by meterological season. PAH were determined by high pressure liquid chromatography (HPLC) with fluorescence and ultraviolet detection. Mutagenicity was measured in the Ames Salmonella bioassay using strain TA98 with and without metabolic activation. The nine-year mean concentration of benzo(a)pyrene (BaP) was 0.4 ng/m3. The mutagenicity of this amount of BaP accounted for only about 0.2% of the observed mutagenicity in POM and other measured PAH accounted for even less. Concentrations of PAH and mutagenicity were three to nine times higher during the winter than during other seasons. Year-to-year wintertime trends in several PAH were also seen. Early in the 1980s, winter concentrations of BaP and benzo (g,h,i)perylene increased. However since the mid-1980's, their concentrations have fallen. The decrease in PAH concentrations may be the result of an increasing proportion of vehicles with relatively low organic emissions. In contrast to PAH, mutagenicity did not show significantly year-to-year time trends.

Air Pollutants↗
PubMedDate not supplied

Unintentional carbon monoxide deaths in California from residential and other nonvehicular sources.

To investigate risk factors of unintentional carbon monoxide deaths in California from nonvehicular sources, we identified 270 deaths resulting from nonvehicular sources of carbon monoxide poisoning from death certificates and coroners' investigation reports. Data recorded between 1979 and 1988 in the state of California on risk factors and carbon monoxide sources were abstracted from investigation reports. We also used census and state statistics to calculate rates and relative risks. The highest rates, which occurred in winter, were found among males, African Americans, and the elderly. Relative risks (in parentheses) were higher among individuals who (a) lived in multiunit dwellings (2.1), (b) dwelled in mobile/trailer homes (4.7), and (c) resided in temporary shelters (30.0) than among individuals who lived in single-family houses (1.0). Unvented combustion heating appliances and charcoal fuel were associated significantly with the risks of fatal unintentional carbon monoxide poisoning.

Accidents↗
PubMedDate not supplied

Umbilical cord blood lead levels in California.

During the fall of 1984, we conducted a survey of umbilical cord blood lead levels of 723 live births that occurred at 5 hospitals located in 5 cities in California. Historical ambient air lead levels were used as a qualitative surrogate of air and dust exposure. The area-specific cord blood means (all means approximately 5 micrograms/dl), medians, deciles, and distributions did not vary among locations. The California distributions included means that were lower than the 6.6 micrograms/dl reported in Needleman et al.'s Boston study in 1979. Indeed, the entire California distribution was shifted to the left of the Boston study distribution, even though 3% of the California cord lead levels exceeded 10 micrograms/dl--the level above which Needleman et al. have documented psychoneurological effects in children during the first few years of life. Fourteen percent of premature babies had cord blood lead levels above 10 micrograms/dl. The association between prematurity (i.e., less than 260 d gestation) and elevated (greater than 5 micrograms/dl) cord blood lead was observed in all hospitals and yielded a relative risk of 2.9 (95% CI: .9, 9.2) and a population attributable risk of 47%. Further research is needed to confirm this association and to explore the roles of endogenous and exogenous sources of lead exposure to the mothers who give birth to premature infants.

Air Pollutants↗