Exposure response, chlorinated

A susceptible population will exhibit a different or enhanced response to chlorine dioxide or chlorite than will most persons exposed to the same level of chlorine dioxide or chlorite in the environment. Reasons may include genetic makeup, age, health and nutritional status, and exposure to other toxic substances (e.g., cigarette smoke). These parameters result in reduced detoxification or excretion of chlorine dioxide or chlorite, or compromised function of organs affected by chlorine dioxide or chlorite. Populations who are at greater risk due to their unusually high exposure to chlorine dioxide or chlorite are discussed in Section 6.7, Populations With Potentially High Exposures. 

Figure 17. Exposure response curves of the chlorinated PMS series.

Chlorine gas is a respiratory irritant and is readily detectable at concentrations of <1 ppm in air because of its penetrating odor. Chlorine gas, after several hours of exposure, causes mild irritation of the eyes and of the mucous membrane of the respiratory tract. At high concentrations and in extreme situations, increased difficulty in breathing can result in death through suffocation. The physiological response to various levels of chlorine gas is given in Table 19. 

The distinctive odor of trichloroethylene may not necessarily provide adequate warning of exposure, because it quickly desensitizes olfactory responses. EataUties have occurred when unprotected workers have entered unventilated areas with high vapor concentrations of trichloroethylene or other chlorinated solvents. Eor a complete description of proper entry to vessels containing any chlorinated solvent, see ASTM D4276-84, Standard Practice for Confined Area Entry (34). 

Only metabolites leached from the cell were affected. Elford and van den Ende reported that ozone at 20 ppm had a lethal effect on some bacteria deposited from aerosol mists on various surfaces. Relative humidity is an important factor, particularly when ozone concentration is low. They found little death at a humidity below 45%, at concentrations of 1 ppm, as opposed to a 90% kill in 30 min at 0.025 ppm with a humidity of around 70%. A 5-min exposure of Bacillus cereus to ozone at 0.12 mg/liter was the minimal lethal dose, whereas 0.10 mg/liter was effective for B. megaterium and E. coli. Spores of the Bacillus sp. were killed by ozone at 2.29 mg/liter. These responses were of the all-or-none type with ozone between 0.4 and 0.5 mg/liter of water. Time of exposure, from 1 to 32 min, was not important. Chlorine was effective at 0.27-0.30 mg/liter, with time an important consideration. These two gases did not affect E. coli in the same way. 

Bherer L, Cushman R, Couteau JP, Quevil-lon M, et al Survey of construction workers repeatedly exposed to chlorine over a three to six month period in a pulpmill II. Follow up of affected workers by questionnaire, spirometry, and assessment of bronchial responsiveness 18 to 24 months after exposure ended. Occup Environ Med 51(4) 225-228, 1994... 

Some studies of occupationally exposed groups have revealed evidence of liver injury by serum enzyme studies or other liver function tests. Adverse effect and dose-effect relationships have not been consistent within and between studies, raising the possibility that other factors (e.g., alcohol intake, other exposures) could be responsible. Review of these studies indicates that some liver effects may have occurred with repeated exposures at concentrations below O.lmg/m assuming RGBs were responsible. Several deaths due to toxic hepatitis have been reported among workers exposed to mixtures of RGBs with chlorinated naphthalenes such effects have not been observed with PGB exposure alone. ... 

Most, if not all, occupational illnesses associated with 2,4,5-T (such as chloracne) have been found to be the result of product contamination with TCDD. TCDD is extremely toxic to animals, and exposure has also been associated with liver function impairment, peripheral neuropathy, personality changes, porphyria cutanea, hypertrichosis, and hyperpigmentation in humans. TCDD is a chlorinated dioxin, one of a large number of related compounds referred to as dioxins it has no functional use and is not intentionally produced. It has been identified as the responsible toxic agent in several industrial disasters, such as accidental releases at Nitro, WV in 1949, and at Seveso, Italy in 1976. " The role of dioxin contaminants must also be considered in the discussion of 2,4,5-T toxicology. 

Apparent photosynthetic rates in plants subjected to SO2 or NO exposures with constant pollutant concentrations, as illustrated in Figure 1, characteristically dropped rapidly upon initiation of treatment to new depressed equilibrium levels which could be maintained for several ho irs. Hydrogen fluoride, conversely, caused CO2 uptake rates to decline more gradually during fumigation. Chlorine, O3 and NO2 exposures induced inhibition rate responses which were intermediate between these... 

These experts collectively have knowledge of chlorine dioxide and chlorite s physical and chemical properties, toxicokinetics, key health end points, mechanisms of action, human and animal exposure, and quantification of risk to humans. All reviewers were selected in conformity with the conditions for peer review specified in Section 104(I)(13) of the Comprehensive Environmental Response, Compensation, and Liability Act, as amended. 

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