Gas and Propane Combustion from Stoves Emits Benzene and Increases Indoor Air Pollution.

Exposure pathways to the carcinogen benzene are well-established from tobacco smoke, oil and gas development, refining, gasoline pumping, and gasoline and diesel combustion. Combustion has also been linked to the formation of nitrogen dioxide, carbon monoxide, and formaldehyde indoors from gas stoves. To our knowledge, however, no research has quantified the formation of benzene indoors from gas combustion by stoves. Across 87 homes in California and Colorado, natural gas and propane combustion emitted detectable and repeatable levels of benzene that in some homes raised indoor benzene concentrations above well-established health benchmarks. Mean benzene emissions from gas and propane burners on high and ovens set to 350 °F ranged from 2.8 to 6.5 µg min-1, 10 to 25 times higher than emissions from electric coil and radiant alternatives; neither induction stoves nor the food being cooked emitted detectable benzene. Benzene produced by gas and propane stoves also migrated throughout homes, in some cases elevating bedroom benzene concentrations above chronic health benchmarks for hours after the stove was turned off. Combustion of gas and propane from stoves may be a substantial benzene exposure pathway and can reduce indoor air quality.

Methane and NOx Emissions from Natural Gas Stoves, Cooktops, and Ovens in Residential Homes.

Natural gas stoves in >40 million U.S. residences release methane (CH4)─a potent greenhouse gas─through post-meter leaks and incomplete combustion. We quantified methane released in 53 homes during all phases of stove use: steady-state-off (appliance not in use), steady-state-on (during combustion), and transitory periods of ignition and extinguishment. We estimated that natural gas stoves emit 0.8-1.3% of the gas they use as unburned methane and that total U.S. stove emissions are 28.1 [95% confidence interval: 18.5, 41.2] Gg CH4 year-1. More than three-quarters of methane emissions we measured originated during steady-state-off. Using a 20-year timeframe for methane, annual methane emissions from all gas stoves in U.S. homes have a climate impact comparable to the annual carbon dioxide emissions of 500 000 cars. In addition to methane emissions, co-emitted health-damaging air pollutants such as nitrogen oxides (NOx) are released into home air and can trigger respiratory diseases. In 32 homes, we measured NOx (NO and NO2) emissions and found them to be linearly related to the amount of natural gas burned (r2 = 0.76; p ≪ 0.01). Emissions averaged 21.7 [20.5, 22.9] ng NOx J-1, comprised of 7.8 [7.1, 8.4] ng NO2 J-1 and 14.0 [12.8, 15.1] ng NO J-1. Our data suggest that families who don't use their range hoods or who have poor ventilation can surpass the 1-h national standard of NO2 (100 ppb) within a few minutes of stove usage, particularly in smaller kitchens.

Composition, Emissions, and Air Quality Impacts of Hazardous Air Pollutants in Unburned Natural Gas from Residential Stoves in California.

The presence of hazardous air pollutants (HAPs) entrained in end-use natural gas (NG) is an understudied source of human health risks. We performed trace gas analyses on 185 unburned NG samples collected from 159 unique residential NG stoves across seven geographic regions in California. Our analyses commonly detected 12 HAPs with significant variability across region and gas utility. Mean regional benzene, toluene, ethylbenzene, and total xylenes (BTEX) concentrations in end-use NG ranged from 1.6-25 ppmv─benzene alone was detected in 99% of samples, and mean concentrations ranged from 0.7-12 ppmv (max: 66 ppmv). By applying previously reported NG and methane emission rates throughout California's transmission, storage, and distribution systems, we estimated statewide benzene emissions of 4,200 (95% CI: 1,800-9,700) kg yr-1 that are currently not included in any statewide inventories─equal to the annual benzene emissions from nearly 60,000 light-duty gasoline vehicles. Additionally, we found that NG leakage from stoves and ovens while not in use can result in indoor benzene concentrations that can exceed the California Office of Environmental Health Hazard Assessment 8-h Reference Exposure Level of 0.94 ppbv─benzene concentrations comparable to environmental tobacco smoke. This study supports the need to further improve our understanding of leaked downstream NG as a source of health risk.

Quantifying Methane Emissions from Natural Gas Water Heaters.

Methane emissions from natural gas appliances remain the least characterized portion of the fossil-fuel supply chain. Here we examine water heaters from 64 northern California homes to (1) quantify methane emissions from natural gas leaks and incomplete combustion while off, turning on or off, and in steady-state operation from 35 homes; and (2) characterize daily usage patterns over ∼1-2 months per water heater to estimate activity factors from 46 homes. Individual tankless water heaters emitted 2390 [95% CI: 2250, 2540] g CH4 yr-1 on average, 0.93% [0.87%, 0.99%] of their natural gas consumed, primarily from on/off pulses. Storage water heaters emitted 1400 [1240, 1560] g CH4 yr-1 on average, 0.39% [0.34%, 0.43%] of their natural gas consumption. Despite higher methane emissions, tankless water heaters generate 29% less CO2e20 than storage water heaters because they use less energy to heat a unit of water. Scaling our measured emissions by the number of storage and tankless water heaters in the United States (56.8 and 1.2 million, respectively), water heaters overall emitted an estimated 82.3 [73.2, 91.5] Gg CH4 yr-1, 0.40% [0.35%, 0.44%] of all natural gas consumed by these appliances, comparable in percentage to the EPA's estimate of methane emissions from upstream natural gas production.

Methane Emissions from Abandoned Oil and Gas Wells in California.

California hosts ∼124,000 abandoned and plugged (AP) oil and gas wells, ∼38,000 idle wells, and ∼63,000 active wells, whose methane (CH4) emissions remain largely unquantified at levels below ∼2 kg CH4 h-1. We sampled 121 wells using two methods: a rapid mobile plume integration method (detection ∼0.5 g CH4 h-1) and a more sensitive static flux chamber (detection ∼1 × 10-6 g CH4 h-1). We measured small but detectable methane emissions from 34 of 97 AP wells (mean emission: 0.286 g CH4 h-1). In contrast, we found emissions from 11 of 17 idle wells-which are not currently producing (mean: 35.4 g CH4 h-1)-4 of 6 active wells (mean: 189.7 g CH4 h-1), and one unplugged well-an open casing with no infrastructure present (10.9 g CH4 h-1). Our results support previous findings that emissions from plugged wells are low but are more substantial from idle wells. In addition, our smaller sample of active wells suggests that their reported emissions are consistent with previous studies and deserve further attention. Due to limited access, we could not measure wells in most major active oil and gas fields in California; therefore, we recommend additional data collection from all types of wells but especially active and idle wells.

Nitrogen dioxide exposure, health outcomes, and associated demographic disparities due to gas and propane combustion by U.S. stoves.

Gas and propane stoves emit nitrogen dioxide (NO2) pollution indoors, but the exposures of different U.S. demographic groups are unknown. We estimate NO2 exposure and health consequences using emissions and concentration measurements from >100 homes, a room-specific indoor air quality model, epidemiological risk parameters, and statistical sampling of housing characteristics and occupant behavior. Gas and propane stoves increase long-term NO2 exposure 4.0 parts per billion volume on average across the United States, 75% of the World Health Organization's exposure guideline. This increased exposure likely causes ~50,000 cases of current pediatric asthma from long-term NO2 exposure alone. Short-term NO2 exposure from typical gas stove use frequently exceeds both World Health Organization and U.S. Environmental Protection Agency benchmarks. People living in residences <800 ft2 in size incur four times more long-term NO2 exposure than people in residences >3000 ft2 in size; American Indian/Alaska Native and Black and Hispanic/Latino households incur 60 and 20% more NO2 exposure, respectively, than the national average.

Chemical Characterization of Natural Gas Leaking from Abandoned Oil and Gas Wells in Western Pennsylvania.

The U.S. Environmental Protection Agency estimates that there are over 3.2 million abandoned wells in the United States. Studies conducted on gas emissions from abandoned wells have been limited to methane, a powerful greenhouse gas, due to concerns regarding climate change. However, volatile organic compounds (VOCs), including benzene, a known human carcinogen, are known to be associated with upstream oil and gas development and hence could also be released when methane is emitted to the atmosphere. In this investigation, we analyze gas from 48 abandoned wells in western Pennsylvania for fixed gases, light hydrocarbons, and VOCs and estimate associated emission rates. We demonstrate that (1) gas from abandoned wells contains VOCs, including benzene; (2) VOCs are emitted from abandoned wells, the magnitude of which depends on the flow rate and concentration of VOCs in the gas stream; and (3) nearly one-quarter of abandoned wells are located within 100 m of buildings, including residences, in Pennsylvania. Together, these observations indicate that further investigation is necessary to determine whether emissions from abandoned wells pose an inhalation risk to people living, working, or congregating near abandoned wells.

Natural gas odorants: A scoping review of health effects.

PURPOSE OF REVIEW: Organosulfur compounds are intentionally added to natural gas as malodorants with the intent of short-term nasal inhalation to aid in leak detection. Regulatory exposure limits have not been established for all commonly used natural gas odorants, and recent community-level exposure events and growing evidence of indoor natural gas leakage have raised concerns associated with natural gas odorant exposures. We conducted a scoping review of peer-reviewed scientific publications on human exposures and animal toxicological studies of natural gas odorants to assess toxicological profiles, exposure potential, health effects and regulatory guidelines associated with commonly used natural gas odorants. RECENT FINDINGS: We identified only 22 studies which met inclusion criteria for full review. Overall, there is limited evidence of both transient nonspecific health symptoms and clinically diagnosed causative neurotoxic effects associated with prolonged odorant exposures. Across seven community-level exposure events and two occupational case reports, consistent symptom patterns included: headache, ocular irritation, nose and throat irritation, respiratory complaints such as shortness of breath and asthma attacks, and skin irritation and rash. Of these, respiratory inflammation and asthma exacerbations are the most debilitating, whereas the high prevalence of ocular and dermatologic symptoms suggest a non-inhalation route of exposure. The limited evidence available raises the possibility that organosulfur odorants may pose health risks at exposures much lower than presently understood, though additional dose-response studies are needed to disentangle specific toxicologic effects from nonspecific responses to noxious organosulfur odors. Numerous recommendations are provided including more transparent and prescriptive natural gas odorant use practices.

Transition from reversible to persistent binding of CaMKII to postsynaptic sites and NR2B.

Changes in protein-protein interactions and activity states have been proposed to underlie persistent synaptic remodeling that is induced by transient stimuli. Here, we show an unusual stimulus-dependent transition from a short-lived to long-lasting binding between a synaptic receptor and its transducer. Both molecules, the NMDA receptor subunit NR2B and Ca2+/calmodulin (CaM)-dependent protein kinase II (CaMKII), are strongly implicated in mediating synaptic plasticity. We show that CaMKII reversibly translocates to synaptic sites in response to brief stimuli, but its resident time at the synapse increases after longer stimulation. Thus, CaMKII localization reflects temporal patterns of synaptic stimulation. We have identified two surface regions of CaMKII involved in short-lived and long-term interactions with NR2B. Our results support an initial reversible and Ca2+/CaM-dependent binding at the substrate-binding site ("S-site"). On longer stimulation, a persistent interaction is formed at the T286-binding site ("T-site"), thereby keeping the autoregulatory domain displaced and enabling Ca2+/CaM-independent kinase activity. Such dual modes of interaction were observed in vitro and in HEK cells. In hippocampal neurons, short-term stimulation initiates a reversible translocation, but an active history of stimulation beyond some threshold produces a persistent synaptic localization of CaMKII. This activity-dependent incorporation of CaMKII into postsynaptic sites may play a role in maturation and plasticity of synapses.

A mechanism for Ca2+/calmodulin-dependent protein kinase II clustering at synaptic and nonsynaptic sites based on self-association.

The activity of Ca2+/calmodulin-dependent protein kinase II (CaMKII) plays an integral role in regulating synaptic development and plasticity. We designed a live-cell-imaging approach to monitor an activity-dependent clustering of green fluorescent protein (GFP)-CaMKII holoenzymes, termed self-association, a process that we hypothesize contributes to the translocation of CaMKII to synaptic and nonsynaptic sites in activated neurons. We show that GFP-CaMKII self-association in human embryonic kidney 293 (HEK293) cells requires a catalytic domain and multimeric structure, requires Ca2+ stimulation and a functional Ca2+/CaM-binding domain, is regulated by cellular pH and Thr286 autophosphorylation, and has variable rates of dissociation depending on Ca2+ levels. Furthermore, we show that the same rules that govern CaMKII self-association in HEK293 cells apply for extrasynaptic and postsynaptic translocation of GFP-CaMKII in hippocampal neurons. Our data support a novel mechanism for targeting CaMKII to postsynaptic sites after neuronal activation. As such, CaMKII may form a scaffold that, in combination with other synaptic proteins, recruits and localizes additional proteins to the postsynaptic density. We discuss the potential function of CaMKII self-association as a tag of synaptic activity.

Translocation of CaMKII to dendritic microtubules supports the plasticity of local synapses.

The processing of excitatory synaptic inputs involves compartmentalized dendritic Ca(2+) oscillations. The downstream signaling evoked by these local Ca(2+) transients and their impact on local synaptic development and remodeling are unknown. Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is an important decoder of Ca(2+) signals and mediator of synaptic plasticity. In addition to its known accumulation at spines, we observed with live imaging the dynamic recruitment of CaMKII to dendritic subdomains adjacent to activated synapses in cultured hippocampal neurons. This localized and transient enrichment of CaMKII to dendritic sites coincided spatially and temporally with dendritic Ca(2+) transients. We show that it involved an interaction with microtubular elements, required activation of the kinase, and led to localized dendritic CaMKII autophosphorylation. This process was accompanied by the adjacent remodeling of spines and synaptic AMPA receptor insertion. Replacement of endogenous CaMKII with a mutant that cannot translocate within dendrites lessened this activity-dependent synaptic plasticity. Thus, CaMKII could decode compartmental dendritic Ca(2+) transients to support remodeling of local synapses.