Extramural papers of the month
By Nancy Lamontagne
- Black carbon from kerosene lamps contributes to climate change
- Bioanalytical tool measures toxicity of bioavailable complex mixtures
- Developing new chemicals free of endocrine disruptors
- Mechanism for increased Parkinson’s disease risk from benomyl exposure
Black carbon from kerosene lamps contributes to climate change
A study, funded in part by NIEHS, shows that the kerosene-fueled wick lamps, commonly used in developing-country households, are a significant source of black carbon emissions. Replacing these lamps with cleaner light sources would benefit people’s health and the planet.
Black carbon contributes to global warming, because it absorbs light and heats the atmosphere. The researchers conducted both field and laboratory testing of kerosene wick lamps, finding that 7 to 9 percent of the kerosene consumed is converted to carbonaceous particulate matter that is nearly pure black carbon. From these emission factors, they estimated that kerosene lighting emits 270,000 metric tons of black carbon per year, a 20-fold increase from previous estimates.
Radiative forcing is a common measure of climate impact that describes the change in Earth’s net energy balance brought on by a constituent(s) at the top of the atmosphere. The researchers estimated the aerosol climate forcing on atmosphere and snow from kerosene wick lamps is 7 percent of black carbon forcing from all other energy-related sources.
Citation: Lam NL, Chen Y, Weyant C, Venkataraman C, Sadavarte P, Johnson MA, Smith KR, Brem BT, Arineitwe J, Ellis JE, Bond TC. 2012. Household light makes global heat: high black carbon emissions from kerosene wick lamps. Environ Sci Technol 46(24):13531-13538. Story
Bioanalytical tool measures toxicity of bioavailable complex mixtures
NIEHS grantees report that a bioanalytical tool, known as Biological Response Indicator Devices Gauging Environmental Stressors (BRIDGES), can detect highly resolved spatial and temporal differences in bioavailable chemicals in the environment, and measure the toxicity of these environmental mixtures.
BRIDGES combines passive sampling and an embryonic zebrafish developmental toxicity bioassay to measure the toxicity of bioavailable complex mixtures. To test the approach, the researchers used passive sampling devices to sequester and concentrate bioavailable organic contaminants in the Willamette and Columbia Rivers within and outside of the Portland Harbor Superfund site in Portland, Ore.
They analyzed extracts from the devices to check for the presence of polycyclic aromatic hydrocarbon (PAH) compounds and 1,201 chemicals of concern using deconvolution-reporting software. The researchers then examined the developmental toxicity of the extracts with the embryonic zebrafish bioassay. Using multivariate modeling, they linked chemicals with toxic effects and identified the PAH analytes most highly correlated with observed toxicity. The researchers say that the BRIDGES tool could be useful for a wide range of environmental monitoring projects.
Citation: Allan SE, Smith BW, Tanguay RL, Anderson KA. 2012. Bridging environmental mixtures and toxic effects. Environ Toxicol Chem 31(12):2877-2887.
Developing new chemicals free of endocrine disruptors
NIEHS grantees and scientists are part of a group of researchers proposing a new Tiered Protocol for Endocrine Disruption (TiPED) for detecting chemicals with possible endocrine disrupting properties. The voluntary protocol could help manufacturers and chemists avoid introducing endocrine disrupting chemicals during product and chemical development.
Endocrine disruptors are found in many consumer products and can lead to developmental, reproductive, neurological, and immune problems. TiPED’s five testing tiers range from broad evaluation based on computer modeling, to specific assays based on cells and whole organisms. The tiers progress in complexity and cost, as well as the reliability of results. A user can use all the tiers or start with any tier in the system.
In a proof-of-principle test, the researchers used TiPED to analyze six endocrine disrupting chemicals, each with different endocrinological mechanisms. Each chemical was identified as endocrine active by one or more tiers. The scientists also established a plan to incorporate new assays into the protocol, as scientific understanding of endocrine disruption continues to advance.
Citation: Schug TT, Abagyan R, Blumberg B, Collins TJ, Crews D, DeFur PL, Dickerson SM, Edwards TM, Gore AC, Guillette LJ, Hayes T, Heindel JJ, Moores A, Patisaul HB, Tal TL, Thayer KA, Vandenberg LN, Warner JC, Watson CS, vom Saal FS, Zoeller RT, O'Brien KP, Myers JP. 2013. Designing endocrine disruption out of the next generation of chemicals. Green Chem 15(1):181-198.
Mechanism for increased Parkinson’s disease risk from benomyl exposure
NIEHS grantees integrated findings from cell, animal, and population studies to reveal how exposure to the fungicide benomyl increases risk for Parkinson's disease. Their work suggests that the neurodegenerative process by which benomyl acts might also occur in people with Parkinson’s disease who were not exposed to benomyl.
Benomyl was discontinued in the U.S. in 2001, but is still used in some countries. The researchers’ population studies indicated an association between higher exposure to benomyl and increased Parkinson’s disease risk. They tested the effects of benomyl on cell cultures, finding that the fungicide inhibited aldehyde dehydrogenase (ALDH) activity and altered dopamine levels. Cell culture experiments and tests using a zebrafish model of Parkinson’s disease showed that benomyl brought on selective loss of dopamine-producing neurons while not affecting other types of neurons. The cell loss decreased when the researchers added an enzyme that reduced the formation of 3,4-dihydroxyphenylacetaldehyde (DOPAL), a reactive dopamine metabolite.
These results, together with those from previous studies, provide evidence for a Parkinson’s disease pathway in which benomyl inhibits ALDH, leading to DOPAL accumulation and degeneration of dopamine-producing neurons. This ALDH pathway may explain why dopamine-producing neurons are selectively vulnerable in Parkinson’s disease and could also provide a new target for therapeutic drugs.
Citation: Fitzmaurice AG, Rhodes SL, Lulla A, Murphy NP, Lam HA, O'Donnell KC, Barnhill L, Casida JE, Cockburn M, Sagasti A, Stahl MC, Maidment NT, Ritz B, Bronstein JM. 2012. Aldehyde dehydrogenase inhibition as a pathogenic mechanism in Parkinson disease. Proc Natl Acad Sci U S A 110(2):636-641. Story
(Nancy Lamontagne is a science writer with MDB, Inc., a contractor for the NIEHS Division of Extramural Research and Training, Superfund Research Program, and Worker Education and Training Program.)