The Effect of Short Term Exposure to Secondhand Smoke at Car/Bar Concentrations on Pulmonary Resistance

This study aimed to estimate the secondhand smoke (SHS) exposure using urinary cotinine (UCo) to prove that the SHS exposure could not be properly assessed by self-reporting (SR). In total, 28,574 nonsmokers aged >19 years were selected from the Korean National Health and Nutrition Examination Survey data (2009–2018). First, changes in the annual concentration of UCo were analyzed, and the annual SHS exposure rates were measured based on SR and UCo from 2009 to 2018. Then, the average UCo concentration and UCo-measured SHS exposure rate were confirmed according to the subjects’ characteristics. Finally, factors associated with the UCo-measured SHS exposure rate were identified based on multiple regression analysis. The findings showed that the annual UCo concentrations and self-reported SHS exposure rates dropped significantly over the past decade. In contrast, the UCo-measured SHS exposure rate indicated that >80% of nonsmokers are still exposed to SHS. Moreover, we found vulnerable groups using UCo-measured SHS exposure rate. In particular, the self-reported SHS exposure at home and in workplaces and house type was highly associated with SHS exposure. Thus, these findings indicate that the actual SHS exposure could not be properly assessed by SR and should be verified using a biomarker, such as UCo. Considering that even a short-term exposure can be harmful to health, the goal of the policy should be to keep cotinine concentration as low as possible.

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Effects of ozone on cyclooxygenase metabolites in the baboon tracheobronchial tree

Journal of Applied Physiology ◽

10.1152/jappl.1990.69.1.245 ◽

1990 ◽

Vol 69 (1) ◽

pp. 245-250 ◽

Cited By ~ 6

Author(s):

J. M. Fouke ◽

R. A. DeLemos ◽

M. J. Dunn ◽

E. R. McFadden

Keyword(s):

Arachidonic Acid ◽

Hydrolysis Product ◽

Tracheobronchial Tree ◽

Ozone Exposure ◽

Base Line ◽

Respiratory Resistance ◽

Pulmonary Resistance ◽

Short Term ◽

Short Term Exposure ◽

Before And After

Short-term exposure to 0.5 parts per million (ppm) ozone has been shown to cause an increase in respiratory resistance in primates that can be diminished by 50% with pretreatment with cromolyn sodium. Because of the known membrane-stabilizing effects of cromolyn and the resultant inhibition of mediator production, we hypothesized a role for the products of arachidonic acid (AA) metabolism in these events. We exposed five adult male baboons to 0.5 ppm ozone on two occasions, once with cromolyn pretreatment and once without. Pulmonary resistance (RL) was monitored and bronchoalveolar lavage (BAL) was performed before and after each exposure. The BAL was analyzed for a stable hydrolysis product of prostacyclin, 6-keto-prostaglandin (PG) F1 alpha, PGE2, a stable hydrolysis product of thromboxane (Tx) A2, TxB2, and PGF2 alpha. RL increased after ozone exposure (1.62 +/- 0.23 to 3.77 +/- 0.51 cmH2O.l-1.s, difference 2.15; P less than 0.02), and this effect was partially blocked by cromolyn (1.93 +/- 0.09 to 3.18 +/- 0.40 cmH2O.l-1.s, difference 1.25; P less than 0.02). The base-line levels of the metabolites of AA in the BAL were as follows (in pg/ml): 6-keto-PGF1 alpha 72.78 +/- 12.6, PGE2 145.92 +/- 30.52, TxB2 52.52 +/- 9.56, and PGF2 alpha 22.28 +/- 5.42. Ozone exposure had no effect on the level of any of these prostanoids (P = NS). These studies quantify the magnitude of cyclooxygenase products of AA metabolism in BAL from baboon lungs and demonstrate that changes in the levels of these mediators in BAL are not prerequisites for ozone-induced increases in respiratory resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

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Utah Kids' Exposure to Secondhand Smoke at All-time Low: UDOH Releases New Findings in 2008 Annual Report

PsycEXTRA Dataset ◽

10.1037/e547832009-001 ◽

2008 ◽

Keyword(s):

Secondhand Smoke ◽

Annual Report ◽

New Findings ◽

Exposure To Secondhand Smoke

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The Effect of Dimethyl Sulfoxide on In Vitro Platelet Function

Thrombosis and Haemostasis ◽

10.1055/s-0038-1648027 ◽

1976 ◽

Vol 36 (01) ◽

pp. 221-229 ◽

Cited By ~ 16

Author(s):

Charles A. Schiffer ◽

Caroline L. Whitaker ◽

Morton Schmukler ◽

Joseph Aisner ◽

Steven L. Hilbert

Keyword(s):

Platelet Count ◽

Platelet Aggregation ◽

Dimethyl Sulfoxide ◽

Platelet Function ◽

Platelet Volume ◽

Short Term ◽

Platelet Factor ◽

Short Term Exposure ◽

Structural Abnormalities

SummaryAlthough dimethyl sulfoxide (DMSO) has been used extensively as a cryopreservative for platelets there are few studies dealing with the effect of DMSO on platelet function. Using techniques similar to those employed in platelet cryopreservation platelets were incubated with final concentrations of 2-10% DMSO at 25° C. After exposure to 5 and 10% DMSO platelets remained discoid and electron micrographs revealed no structural abnormalities. There was no significant change in platelet count. In terms of injury to platelet membranes, there was no increased availability of platelet factor-3 or leakage of nucleotides, 5 hydroxytryptamine (5HT) or glycosidases with final DMSO concentrations of 2.5, 5 and 10% DMSO. Thrombin stimulated nucleotide and 5HT release was reduced by 10% DMSO. Impairment of thrombin induced glycosidase release was noted at lower DMSO concentrations and was dose related. Similarly, aggregation to ADP was progressively impaired at DMSO concentrations from 1-5% and was dose related. After the platelets exposed to DMSO were washed, however, aggregation and release returned to control values. Platelet aggregation by epinephrine was also inhibited by DMSO and this could not be corrected by washing the platelets. DMSO-plasma solutions are hypertonic but only minimal increases in platelet volume (at 10% DMSO) could be detected. Shrinkage of platelets was seen with hypertonic solutions of sodium chloride or sucrose suggesting that the rapid transmembrane passage of DMSO prevented significant shifts of water. These studies demonstrate that there are minimal irreversible alterations in in vitro platelet function after short-term exposure to DMSO.

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Cancer of the Lung, Larynx, and Pleura

10.1093/oso/9780190676827.003.0014 ◽

2018 ◽

Author(s):

Jyoti Malhotra ◽

Paolo Boffetta ◽

Lorelei Mucci

Keyword(s):

Lung Cancer ◽

Secondhand Smoke ◽

Lung Cancer Risk ◽

Occupational Exposures ◽

Men And Women ◽

Established Risk Factor ◽

Former Smokers ◽

Never Smokers ◽

Exposure To Secondhand Smoke ◽

Cancer Of The Lung

Lung cancer is the most commonly diagnosed cancer among men in most countries, and is the primary cause of cancer death in men and women. Its epidemic increase in incidence began in the first half of the twentieth century, paralleling the uptake of cigarette smoking that occurred 20 years before. A series of landmark studies beginning in 1950 established tobacco as the primary cause of lung cancer. Current smokers have a 10- to 20-fold higher lung cancer risk compared to never smokers. Important for prevention, former smokers substantially reduce this excess risk 5 years after smoking cessation. Exposure to secondhand smoke, a well-established risk factor for lung cancer, has a 20%–25% higher risk for those exposed. There are several occupational exposures associated with lung cancer, including asbestos. Despite the success in defining lung cancer’s etiology, this highly preventable disease remains among the most common and most lethal cancers globally.

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