Consumer, industrial, and commercial product usage is a source of exposure to potentially hazardous chemicals. In addition, cleaning agents, personal care products, coatings, and other volatile chemical products (VCPs), evaporate and react in the atmosphere producing secondary pollutants. Here, we show high air emissions from VCP usage (≥ 14 kg person
−1
yr
−1
, at least 1.7× higher than current operational estimates) are supported by multiple estimation methods and constraints imposed by ambient levels of ozone, hydroxyl radical (OH) reactivity, and the organic component of fine particulate matter (PM
2.5
) in Pasadena, California. A near-field model, which estimates human chemical exposure during or in the vicinity of product use, indicates these high air emissions are consistent with organic product usage up to ~75 kg person
−1
yr
−1
, and inhalation of consumer products could be a non-negligible exposure pathway. After constraining the PM
2.5
yield to 5% by mass, VCPs produce ~41% of the photochemical organic PM
2.5
(1.1 ± 0.3
μ
g m
−3
) and ~17% of maximum daily 8-hr average ozone (9 ± 2 ppb) in summer Los Angeles. Therefore, both toxicity and ambient criteria pollutant formation should be considered when organic substituents are developed for VCPs in pursuit of safer and sustainable products and cleaner air.
Abstract. We describe simulations using an updated version of the
Community Multiscale Air Quality model version 5.3 (CMAQ v5.3) to
investigate the contribution of intermediate-volatility organic compounds
(IVOCs) to secondary organic aerosol (SOA) formation in southern California
during the CalNex study. We first derive a model-ready parameterization for
SOA formation from IVOC emissions from mobile sources. To account for SOA
formation from both diesel and gasoline sources, the parameterization has
six lumped precursor species that resolve both volatility and molecular
structure (aromatic versus aliphatic). We also implement new mobile-source
emission profiles that quantify all IVOCs based on direct measurements. The
profiles have been released in SPECIATE 5.0. By incorporating both
comprehensive mobile-source emission profiles for semivolatile organic compounds (SVOCs) and IVOCs and
experimentally constrained SOA yields, this CMAQ configuration best
represents the contribution of mobile sources to urban and regional ambient
organic aerosol (OA). In the Los Angeles region, gasoline sources emit 4 times more
non-methane organic gases (NMOGs) than diesel sources, but diesel emits
roughly 3 times more IVOCs on an absolute basis. The revised model predicts
all mobile sources (including on- and off-road gasoline, aircraft, and on-
and off-road diesel) contribute ∼1 µg m−3 to the
daily peak SOA concentration in Pasadena. This represents a ∼70 % increase in predicted daily peak SOA formation compared to the base
version of CMAQ. Therefore, IVOCs in mobile-source emissions contribute
almost as much SOA as traditional precursors such as single-ring aromatics.
However, accounting for these emissions in CMAQ does not reproduce
measurements of either ambient SOA or IVOCs. To investigate the potential
contribution of other IVOC sources, we performed two exploratory simulations
with varying amounts of IVOC emissions from nonmobile sources. To close the
mass balance of primary hydrocarbon IVOCs, IVOCs would need to account for
12 % of NMOG emissions from nonmobile sources (or equivalently 30.7 t d−1 in the Los Angeles–Pasadena region), a value that is well within
the reported range of IVOC content from volatile chemical products. To close
the SOA mass balance and also explain the mildly oxygenated IVOCs in
Pasadena, an additional 14.8 % of nonmobile-source NMOG emissions would
need to be IVOCs (assuming SOA yields from the mobile IVOCs apply to
nonmobile IVOCs). However, an IVOC-to-NMOG ratio of 26.8 % (or
equivalently 68.5 t d−1 in the Los Angeles–Pasadena region) for
nonmobile sources is likely unrealistically high. Our results highlight the
important contribution of IVOCs to SOA production in the Los Angeles region but underscore that other uncertainties must be addressed (multigenerational
aging, aqueous chemistry and vapor wall losses) to close the SOA mass
balance. This research also highlights the effectiveness of regulations to
reduce mobile-source emissions, which have in turn increased the relative
importance of other sources, such as volatile chemical products.
During the COVID-19 lockdown period (from January 23 to February 29, 2020), ambient
PM
2.5
concentrations in the Yangtze River Delta (YRD) region were observed
to be much lower, while the maximum daily 8 h average (MDA8) O
3
concentrations became much higher compared to those before the lockdown (from January 1
to 22, 2020). Here, we show that emission reduction is the major driving force for the
PM
2.5
change, contributing to a PM
2.5
decrease by 37% to 55% in
the four YRD major cities (i.e., Shanghai, Hangzhou, Nanjing, and Hefei), but the MDA8
O
3
increase is driven by both emission reduction (29%–52%) and
variation in meteorological conditions (17%– 49%). Among all pollutants,
reduction in emissions mainly of primary PM contributes to a PM
2.5
decrease
by 28% to 46%, and NOx emission reduction contributes 7% to 10%. Although NOx emission
reduction dominates the MDA8 O
3
increase (38%–59%), volatile organic
compounds (VOCs) emission reduction lead to a 5% to 9% MDA8 O
3
decrease.
Increased O
3
promotes secondary aerosol formation and partially offsets the
decrease of PM
2.5
caused by the primary PM emission reductions. The results
demonstrate that more coordinated air pollution control strategies are needed in
YRD.
Changes in tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-10 and vascular endothelial growth factor (VEGF) in serum and bronchoalveolar lavage fluid (BALF) in rats with acute respiratory distress syndrome (ARDS) and the intervention effect of dexamethasone were observed to explore the theoretical basis of dexamethasone in the treatment of ARDS. Seventy-two rats were randomly divided into normal control group (group N, n=24), ARDS model group (group L, n=24) and dexamethasone group (group D, n=24). The ARDS rat model was established by jointly injecting oleic acid and lipopolysaccharide via the caudal vein, while rats in group D received intervention with dexamethasone. The wet/dry weight ratios of lung tissues were measured, and the levels of TNF-α, IL-6, IL-10 and VEGF in serum and BALF were measured via enzyme-linked immunosorbent assay. The wet/dry weight ratio of lung tissues of rats in group D was significantly decreased compared with that in group L (P<0.05 or P<0.01). The levels of TNF-α, IL-6 and VEGF in serum and BALF of rats in group L and D were obviously increased compared with those in group N at each time point (P<0.01). The levels of TNF-α, IL-6 and VEGF in serum and BALF of rats in group D were significantly decreased compared with those in group L (P<0.01). In conclusion, there is a serious imbalance between anti-inflammatory response and inflammatory response in rats with ARDS induced by oleic acid combined with lipopolysaccharide of Escherichia coli, whereas dexamethasone can alleviate lung injury through inhibiting expression levels of inflammatory factors and promoting expression levels of anti-inflammatory factors.
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