Phosgene Poisoning Caused by the Use of Chemical Paint Removers Containing Methylene Chloride in Ill-Ventilated Rooms Heated by Kerosene Stoves

Gerritsen, Wim B.; Buschmann, Christoph

doi:10.1136/oem.17.3.187

Cited by 14 publications

(7 citation statements)

References 1 publication

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“…Popular Mechanics ( Triuni, 1983 ) suggests that proper ventilation for paint stripping requires an air flow rate of 10 ±15 ACH, which can typically only be attained with an exhaust fan ( Popular Mechanics recommends air delivery of at least 500 ft 3 /min, or 850 m 3 /h). Unfortunately, many paint strippers are flammable, so that a spark from a normal house fan could set off a fire or explosion, which could be particularly hazardous since phosgene is a by -product of the combustion of methylene chloride (Gerritsen and Buschmann, 1960 ).…”

Section: Discussionmentioning

confidence: 99%

Modeling methylene chloride exposure-reduction options for home paint-stripper users

Riley

Small

Fischhoff

2000

J Expo Sci Environ Epidemiol

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Home improvement is a popular activity, but one that can also involve exposure to hazardous substances. Paint stripping is of particular concern because of the high potential exposures to methylene chloride, a solvent that is a potential human carcinogen and neurotoxicant. This article presents a general methodology for evaluating the effectiveness of behavioral interventions for reducing these risks. It doubles as a model that assesses exposure patterns, incorporating user time ± activity patterns and risk -mitigation strategies. The model draws upon recent innovations in indoor air -quality modeling to estimate exposure through inhalation and dermal pathways to paint -stripper users. It is designed to use data gathered from home paint -stripper users about room characteristics, amount of stripper used, time ± activity patterns and exposure -reduction strategies ( e.g., increased ventilation and modification in the timing of stripper application, scraping, and breaks ) . Results indicate that the effectiveness of behavioral interventions depends strongly on characteristics of the room ( e.g., size, number and size of doors and windows, base air -exchange rates ) . The greatest simple reduction in exposure is achieved by using an exhaust fan in addition to opening windows and doors. These results can help identify the most important information for product labels and other risk -communication materials.

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Section: Discussionmentioning

confidence: 99%

Modeling methylene chloride exposure-reduction options for home paint-stripper users

Riley

Small

Fischhoff

2000

J Expo Sci Environ Epidemiol

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“…It is known to induce noncardiogenic pulmonary edema upon acute inhalation exposure Pawlowski and Frosolono, 1977;Diller et al, 1985). Although environmental levels are relatively low, reaching to about 60 parts per trillion in the urban areas such as Los Angeles, occupational hazards resulting from accidental exposure are well known (Galdston et al, 1947;Gerritsen and Buschmann, 1960;Sjogren et al, 1991). Likewise, emissions from industrial facilities may pose episodic risks to the public living nearby (Davis et al, 1989).…”

mentioning

confidence: 99%

Pulmonary Structural and Extracellular Matrix Alterations in Fischer 344 Rats Following Subchronic Phosgene Exposure

Kodavanti¹,

Costa²,

Giri

et al. 1997

Toxicol Sci

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Phosgene, an acylating agent, is a very potent inducer of pulmonary edema. Subchronic effects of phosgene in laboratory animals are not well characterized. The purpose of the study was to elucidate potential long-term effects on collagen and elastin metabolism during pulmonary injury/recovery and obtain information about the concentration X time (C X T) behavior of low levels of phosgene. Male Fischer 344 rats (60 days old) were exposed either to clean air or phosgene, 6 hr/day: 0.1 ppm (5 days/week), 0.2 ppm (5 days/week), 0.5 ppm (2 days/week), and 1.0 ppm (1 day/week), for 4 or 12 weeks. A group of rats was allowed clean air recovery for 4 weeks after 12 weeks of phosgene exposure. This exposure scenario was designed to provide equal C x T product for all concentrations at one particular time point except for 0.1 ppm (50% C X T). Phosgene exposure for 4 or 12 weeks increased lung to body weight ratio and lung displacement volume in a concentration-dependent manner. The increase in lung displacement volume was significant even at 0.1 ppm phosgene at 4 weeks. Light microscopic level histopathology examination of lung was conducted at 0.0, 0.1, 0.2, and 1.0 ppm phosgene following 4 and 12 and 16 weeks (recovery). Small but clearly apparent terminal bronchiolar thickening and inflammation were evident with 0.1 ppm phosgene at both 4 and 12 weeks. At 0.2 ppm phosgene, terminal bronchiolar thickening and inflammation appeared to be more prominent when compared to the 0.1 ppm group and changes in alveolar parenchyma were minimal. At 1.0 ppm, extensive inflammation and thickening of terminal bronchioles as well as alveolar walls were evident. Concentration rather than C X T seems to drive pathology response. Trichrome staining for collagen at the terminal bronchiolar sites indicated a slight increase at 4 weeks and marked increase at 12 weeks in both 0.2 and 1.0 ppm groups (0.5 ppm was not examined), 1.0 ppm being more intense. Wholelung prolyl hydroxylase activity and hydroxyproline, taken as an index of collagen synthesis, were increased following 1.0 ppm phosgene exposure at 4 as well as 12 weeks, respectively. Desmosine levels, taken as an index of changes in elastin, were increased in the lung after 4 or 12 weeks in the 1.0 ppm phosgene group. Following 4 weeks of air recovery, lung hydroxyproline was further increased in 0.5 and 1.0 ppm phosgene groups. Lung weight also remained significantly higher than the controls; however, desmosine and lung displacement volume in phosgene-exposed animals were similar to controls. In summary, terminal bronchiolar and lung volume displacement changes occurred at very low phosgene concentrations (0.1 ppm). Phosgene concentration, rather than C X T product appeared to drive toxic responses. The changes induced by phosgene (except of collagen) following 4 weeks were not further amplified at 12 weeks despite continued exposure. Phosgene-induced alterations of matrix were only partially reversible after 4 weeks of clean air exposure, c 1997 sod«y or To

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“…In 1987, the estimated annual usage in the United States was over 1 million metric tons (17). In addition, phosgene can be formed by the thermal decomposition of chlorinated hydrocarbons during res (1,7). As a result of this extensive usage, thousands of chemical and industrial workers, welders, and remen are potentially at risk of exposure to phosgene, which can cause life-threatening and latent, noncardiogenic pulmonary edema that often is not seen until 6 to 24 hours after exposure (5).…”

Section: Introductionmentioning

confidence: 99%

Acute Changes in Lung Histopathology and Bronchoalveolar Lavage Parameters in Mice Exposed to the Choking Agent Gas Phosgene

Duniho¹,

Martin²,

Forster³

et al. 2002

Toxicol Pathol

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Phosgene (CG) is a highly irritant gas widely used industrially as a chemical intermediate for the production of dyes, pesticides, and plastics, and can cause life-threatening pulmonar y edema within 24 hours of exposure. This study was designed to investigate acute changes in lung tissue histopathology and selected bronchoalveola r lavage uid (BALF) factors over time to determine early diagnostic indicators of exposure. Three groups of 40 male mice each were exposed to 32 mg/m 3 (8 ppm) CG for 20 minutes, and 3 groups of 40 control male mice were exposed to ltered room air for 20 minutes, both exposures were followed by room air washout for 5 minutes. At 1,4,8,12,24, 48, and 72 hours after exposure each group of mice was euthanized and processed for histopatholog y, bronchoalveola r lavage or gravimetric measurements , respectively. Over time, the histopathologica l lesions were characterized by acute changes consisting of alveolar and interstitial edema, brin and hemorrhage , followed by signi cant alveolar and interstitial ooding with in ammatory cell in ltrates and scattered bronchiolar and terminal airway epithelial degeneratio n and necrosis. From 48 to 72 hours, there was partial resolution of the edema and degenerative changes, followed by epithelial and broblastic regeneration centered on the terminal bronchiolar areas. Bronchoalveola r lavage was processed for cell differential counts, LDH, and protein determination. Comparative analysis revealed signi cant increases in both postexposur e lung wet/dry weight ratios, and early elevations of BALF LDH and protein, and later elevations in leukocytes. This article describes the use of histopathology to chronicle the temporal pulmonary changes subsequent to whole body exposure to phosgene , and correlate these changes with BALF ingredients and postexposur e lung wet weights in an effort to characterize toxic gas-induced acute lung injury and identify early markers of phosgene exposure.

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Phosgene Poisoning Caused by the Use of Chemical Paint Removers Containing Methylene Chloride in Ill-Ventilated Rooms Heated by Kerosene Stoves

Cited by 14 publications

References 1 publication

Modeling methylene chloride exposure-reduction options for home paint-stripper users

Modeling methylene chloride exposure-reduction options for home paint-stripper users

Pulmonary Structural and Extracellular Matrix Alterations in Fischer 344 Rats Following Subchronic Phosgene Exposure

Acute Changes in Lung Histopathology and Bronchoalveolar Lavage Parameters in Mice Exposed to the Choking Agent Gas Phosgene

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