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Appendix 16 Proposed Occupational Exposure Standard
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- ATTACHMENT 1
- ATTACHMENT 2
- Basis for s e tting the limit
- Identity a n d properties of gaseous formalde h yde
- Occurrence and uses
- Occupatio n al exposure
- Workplace air monitoring metho d s
- Toxicoki n etics
- Health effects
Appendix 16Proposed Occupational Exposure StandardThe following documents will serve as attachments to the Regulatory Impact Statement (RIS) when the proposed national occupational exposure standard is released for public comment by OASCC. ATTACHMENT 1Proposed National Occupational Exposure Standard Released for Public Comment OASCC current exposure standard Proposed exposure standard TWA STEL TWA STEL
1.2 mg/m3
2.4 mg/m3 0.3 ppm
0.36 mg/m3 0.6 ppm
0.72 mg/m3 TWA = the average airborne concentration of a particular substance when calculated over a normal eight-hour working day, for a five-day working week. STEL = a 15 minute TWA exposure which should not be exceeded at any time during a working day even if the 8- hour TWA average is within the TWA exposure standard. Exposures at the STEL should not be longer than 15 minutes and should not be repeated more than 4 times per day. There should be at least 60 minutes between successive exposures at the STEL. According to the measured data summarised in the NICNAS Priority Existing Chemical assessment report on formaldehyde, the average levels of formaldehyde around workers’ breathing zone in a number of major use scenarios (long-term and short-term personal sampling) are: Major Use Scenario Exposure (ppm) Long-term Short-term Formaldehyde manufacture Most ≤0.2 0.5 ppm (one sample only) Resin manufacture Most ≤0.2 Most ≤0.5 Product formulation (limited data) Most ≤0.2 Up to 2 Pressed wood product manufacture Most ≤0.3 No data Wood working industry using particleboard and MDF Most < 0.2 No data Forensic/hospital mortuaries & pathology laboratories Most ≤ 0.3 (up to 3) No data
Embalming Most > 0.5 (up to 3.9) Up to 1.4 (limited data) MDF, medium density fibreboard. ATTACHMENT 2Summary Information to Support the Proposed Occupational Exposure Standard [Source: NICNAS Priority Existing Chemical Assessment Report onFormaldehyde] Proposed exposure standard
STEL: 0.6 ppm (0.72 mg/m3) Skin sensitiser The information below has been taken from the National Industrial Chemicals Notification and Assessment Scheme’s (NICNAS) Priority Existing Chemical Assessment Report Number 28 on Formaldehyde. Basis for setting the limitSection 11, 16, 18.3 of the Priority Existing Chemical report Based on the review of the available human and animal data, the critical health effect for setting the occupational exposure standard is sensory irritation. Although formaldehyde is a known eye and upper respiratory tract irritant in humans, the limitations of the available data and subjective nature of sensory irritation do not allow identification of a definitive no- observed-effect level (NOEL). However, the data from chamber studies demonstrates that the sensory irritation responses at levels of ≥1 ppm (1.2 mg/m3) can definitely be attributed to formaldehyde. Some individuals begin to sense irritation from 0.5 ppm (0.6 mg/m3), although the response rate is often similar to that reported in controls. Although there is limited evidence that some individuals report sensory irritation as low as 0.25 ppm (0.3 mg/m3), the data is very unreliable. Therefore, the lowest-observed-effect level (LOEL) is considered to be 0.5 ppm. Data for asthmatics, who are generally thought to be sensitive to irritants, indicate that they are likely to be no more sensitive than non-asthmatics. This is supported by the absence of direct effects of formaldehyde on pulmonary function in asthmatics in these studies. In order to protect the majority of workers from sensory irritation, the recommended exposure standard should be a concentration that is a lower than the LOEL identified. As this is a reversible effect and is generally mild at 0.5 ppm, the standard should be slightly lower than the LOEL. For these reasons the recommended exposure standard is 0.3 ppm TWA and 0.6 ppm STEL. At this level, the nasal cancer risk can be also managed. Furthermore, the recommended exposure standards are consistent with best practice overseas and appear technically achievable in most Australian workplaces (based on industry information submitted for this report). Identity and properties of gaseous formaldehydeSection 4 and 5 of the Priority Existing Chemical report CAS number: 50-00-0 EINECS number: 200-001-8 Formula: CH2O Synonyms: Formalin Vapour pressure: 516 kPa at 25oC Melting point: -118 to -92 oC Solubility: 400 to 550 g/L at 25oC Conversion factor: 1 ppm = 1.2 mg/m3 Formaldehyde is a colourless gas with a pungent, irritating odour at room temperature. The odour threshold of formaldehyde varies widely ranging from 0.05 to 1 ppm. However, for most people, the odour threshold is in the 0.5 to 1 ppm range. Formaldehyde is readily soluble in water, alcohol, and other polar solvents. Formaldehyde is generally available as a 37% to 54% (by weight) aqueous solution, known as formalin. Occurrence and usesSection 7 of the Priority Existing Chemical report Formaldehyde occurs naturally in the environment, with numerous sources of emission, primarily due to the combustion of organic materials and a variety of natural and human activities including bush fires, animal wastes, plant emissions and both direct and indirect combustion processes. Formaldehyde is also naturally present in the human body at very low concentrations, as a result of various metabolic processes. Based on 2000-2002 data, approximately 55 000 tonnes formaldehyde per year (calculated as 100% formaldehyde) is manufactured in Australia as formalin solutions. It is also imported as formalin and products/mixtures containing formaldehyde at approximately 90 tonnes a year. Paraformaldehyde, a significant source of formaldehyde, is imported at around 700 tonnes a year as either pure material or mixtures containing paraformaldehyde. The main industrial use of formalin is for the manufacture of formaldehyde-based resins. These resins are widely used in a variety of industries, predominantly pressed wood manufacture. The majority of the formaldehyde-based resins contain < 0.2% free formaldehyde, but some can contain up to 13%. Formalin is also used directly or in blends in a number of industries including hospitals, mortuaries, medicine-related laboratories, embalming in funeral homes, film processing, leather tanning, and a wide range of personal care and consumer products. The concentrations of formaldehyde in these products range from 40%, such as embalming and film processing solutions, to < 0.2%, for example, the majority of cosmetics and consumer products. Formaldehyde also has agricultural and pharmaceutical uses. Occupational exposureSection 15 of the Priority Existing Chemical report It is estimated that there are approximately 120 potentially exposed workers in formaldehyde and formaldehyde-based resin manufacturing industry at the four manufacturing sites in Australia. Occupational exposure during formaldehyde manufacturing is generally low due to full containment in enclosed systems. There is no information available on the total number of workers who are potentially exposed to formaldehyde during use of products containing formaldehyde in a wide range of industry categories. The levels of formaldehyde exposure based on measured data, although limited for most industries, are summarised as follows: Long-term (TWA) exposures (personal monitoring data) are:
Short-term exposures (personal monitoring data) are:
Workplace air monitoring methodsSection 6 of the Priority Existing Chemical report A number of sampling and analytical methods are available for measuring formaldehyde in air at the workplace. An air sample can be obtained by a filter and impinges, solid sorbent tube or cartridge and quantified by spectrometry, high performance liquid chromatography (HPLC) or gas chromatography. Other methods, such as passive sampler/monitor followed by chromotropic acid test and gas tube detector with infrared analysers, are also used in Australia. Instantaneous measurement of the concentration of airborne formaldehyde by direct read, hand-held electronic formaldehyde devices is commonly used in Australia, for example, formaldehyde meters and Interscan machines. ToxicokineticsSection 9 of the Priority Existing Chemical report Formaldehyde is readily absorbed at the site of contact by all exposure routes due to its high reactivity with biological macromolecules, high water solubility and low molecular weight . It is rapidly metabolised after absorption, with a half-life of about 1 to 1.5 minutes in blood circulation following intravenous administration in animals. Formaldehyde is metabolised to formate by a number of widely distributed cellular enzymes in which formaldehyde dehydrogenase is the most important one. A minor pathway for formaldehyde metabolism is oxidisation to formic acid by the enzyme catalase. Due to the rapid metabolism of formaldehyde, much of the material is expired in air shortly after exposure, and as formate in urine. Health effectsAnimal studies Section 10 of the Priority Existing Chemical report Following acute exposure via inhalation, dermal and oral routes, formaldehyde is moderately toxic in animals. Formaldehyde solution is known to be a skin and eye irritant and strong sensitiser in animals. Following repeated inhalation exposure, the target organ is the nasal tract where the observed effects include alterations in mucociliary clearance, cell proliferation and histopathological changes (cytotoxicity and hyperplasia) to the nasal epithelium at doses ≥2 ppm. The principal non-neoplastic effect observed in animals after repeated oral dosing is irritation at the site of contact (i.e. fore- and glandular-stomach). The limited data available on the repeated dermal toxicity of formaldehyde solution indicate skin irritation and no evidence of systemic toxicity. Formaldehyde is genotoxic in vitro, and it appears that the chemical may be genotoxic at the site of contact in vivo. A significantly increased incidence of nasal squamous cell carcinomas was observed in rats exposed by long-term inhalation at concentrations > 6 ppm formaldehyde. However, these were not observed in mice and hamsters at equivalent or greater exposure concentrations. The available data in animals do not support formaldehyde being carcinogenic by the dermal or oral routes. Limited data indicated that formaldehyde does not produce reproductive or developmental effects in animals. Human data Section 11 of the Priority Existing Chemical report There are old reports of human deaths following ingestion of formaldehyde. Recent cases reported ulceration and damage along the aero-digestive tract that needed surgical operations following ingestion of approximately 700 mg/kg of formaldehyde solution. Sensory irritation has been reported in human epidemiological and chamber studies following inhalation exposure to formaldehyde. However, the limitations of the available data and subjective nature of sensory irritation do not allow identification of a definitive no-observed- effect level (NOEL). The chamber studies suggest that sensory irritation definitely occurs at > 1 ppm (> 1.2 mg/m3) with some individuals beginning to sense irritation from 0.5 ppm (0.6 mg/m3) (Bender, 2002). Although asthmatics are thought to be more sensitive to irritants, studies by Green et al. (1987), Sauder et al. (1986; 1987) and Witek et al. (1987) have demonstrated that at concentrations of 2 to 3 ppm (2.4 to 3.6 mg/m3) for up to 3 hours, asthmatics were not particularly sensitive to formaldehyde. Skin sensitisation by formaldehyde solution is clearly observed in numerous clinical trials and case reports in humans. Epidemiology data from occupational studies investigating cytogenetic effects in nasal and buccal cells are suggestive of formaldehyde having a weak localised genotoxic activity, while the evidence for a systemic activity, including peripheral lymphocytes, is equivocal. Many epidemiology studies have investigated formaldehyde exposure and cancers of the respiratory tract. The strongest evidence of an association has been observed for nasopharnygeal cancers. The most recent meta-analysis (Collins et al., 1997) concluded that although there was an increased, non-significant risk of nasopharyngeal cancers, overall, the data did not provide sufficient evidence to establish a causal relationship between nasopharyngeal cancers and formaldehyde exposure. Studies published since the meta- analysis provide mixed results for both case-control studies and cohort studies. Three large industrial cohort studies with a long follow-up have been recently published (Hauptman et al. 2004, Pinkerton et al., 2004 and Coggon et al., 2003). The study by Hauptman et al. (2004) found that compared to the national population, there was a significantly increase risk of nasopharyngeal cancer. In addition, the relative risk increased with average exposure intensity, cumulative exposure, highest peak exposure and duration of exposure to formaldehyde. However, no such cancers were seen in the study by Pinkerton et al. (2004), while no increased risk was seen by Coggon et al. (2003). Similarly, mixed results have been observed in recent case-control studies of formaldehyde exposure and nasopharyngeal cancer. Overall, although it cannot be definitely concluded that occupational formaldehyde exposure results in the development of nasopharyngeal cancer, there is some evidence to suggest a causal association between formaldehyde exposure and nasopharyngeal cancer. In addition, the postulated mode of action is considered likely to be relevant to humans and is biological plausible. Therefore, based on the available nasopharyngeal cancer data, formaldehyde should be regarded as if it may be carcinogenic to humans following inhalation exposure. There are several case-control studies that indicate an increased risk for sinonasal cancer and formaldehyde exposure, but this has not been observed in cohort studies. The most recent meta-analysis (Collins et al., 1997) concluded that the data did not suggest an association between formaldehyde and sinonasal cancer. There is limited and inconsistent evidence with respect to laryngeal and lung cancers. Overall, the available data do not support an association between sinonasal, laryngeal and lung cancers and formaldehyde exposure. An increased risk of leukaemia, occasionally significant, has been inconsistently reported in human epidemiology studies. The available data do not allow construction of a dose-response relationship for formaldehyde exposure and incidence of leukaemia. Additionally, there is currently no biologically plausible mode of action to explain why formaldehyde would be leukaemogenic. Overall, the available human and animal data are insufficient to establish an association between formaldehyde exposure and leukaemia. Based on animal and limited epidemiology data, formaldehyde is unlikely to cause reproductive and developmental effects at exposures relevant to humans. ReferencesBender, J. (2002) The use of non-cancer endpoints as a basis for establishing a reference concentration for formaldehyde. Regul. Toxicol. Pharmacol. 35:23-31. Blair, A , Saracci R, Steward PA, Hayes RB and Shy C (1990) Epidemiological evidence on the relationship between formaldehyde exposure and cancer. Scandanavian Journal of Work, Environment and Health ,16:381-393. Coggon, D, Harris CE, Poole J and Palmer KT (2003) Extended follow-up of a cohort of British chemical workers exposed to formaldehyde. Journal of the National Cancer Institute, 95 (21): 1608 – 1614. Collins, JJ Aquavella JF; and Esmen NA (1997) An updated meta-analysis of formaldehyde exposure and upper respiratory tract cancer. JOEM. 39:639-651. Green DJ, Saunder LR, Kulle TJ and Bascom R. (1987) Acute responses to 3.0 ppm formaldehyde in exercising healthy nonsmokers and asthmatics. Am Rev Respir Dis. 135:1261-1266. Hauptmann M, Lubin JH, Stewart PA, Hayes RB and Blair A (2003) Mortality from lymphohematopoietic malignancies among workers in formaldehyde industries. Journal of the National Cancer Institute. 95(21):1615-1623. Hauptmann A, Lubin JH, Stewart PA, Hayes RB and Blair A (2004). Mortality from solid cancers among workers in formaldehyde industries. American Journal of Epidemiology, 159(12): 1117-30. Heck H, Chin TY, Schmitz MC (1983) Distribution of [14C]formaldehyde in rats after inhalation exposure. In: Gilbson JE ed. Formaldehyde toxicity. Washington, DC, Hemisphere publishing, pp 26-37. Partanen, T (1993) Formaldehyde exposure and respiratory cancer - a meta-analysis of the epidemiological evidence. Scandanavian Journal of Work, Environment and Health, 19:8-15. Pinkerton, LE, Hein M.J and Stayner LT (2004). Mortality among a cohort of garment workers exposed to formaldehyde: an update. Occupational and Environmental Medicine, 61(3): 193 – 200. Sauder LR, Chatham MD, Green DJ, and Kulle TJ (1986) Acute pulmonary response to formaldehyde exposure in healthy nonsmokers. Journal of Occupational Medicine. 28(6):420- 424. Sauder LR, Green DJ, Chatham MD, and Kulle TJ (1987) Acute pulmonary response of asthmatics to 3.0 ppm formaldehyde. Toxicology and Industrial Health. 3(4): 569-577. Witek TJ Jr, Schachter EN, Tosun T, Beck GJ, and Leaderer BP (1987) An evaluation of respiratory effects following exposure to 2.0 ppm formaldehyde in asthmatics: Lung function, symptoms, and airway reactivity. Archives of Environmental Health, 42: 230-237. 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