Clima político y contexto social en los dos primeros tercios del siglo XX en Chile XX en Chile

Virginia Murray and Ishani Kar-Purkayastha

Learning outcomes

At the end of this chapter and any recommended reading the student should be able to:

1. understand the importance of occupational toxicology in relation to health pro-tection activities;

2. be aware of important sources of information about toxic agents in the workplace;

3. discuss the methods by which occupational exposure to toxic substances may affect health during manufacture, transport, storage, and use;

4. critically discuss incidents that have resulted from occupational exposures to toxic chemicals, and understand how they are investigated;

5. evaluate the guidelines and protocols that are used to prevent or minimize ill-health due to occupational exposures, and

6. apply acquired knowledge in the analysis and management of hazardous situations.

8.1

Introduction

Occupational toxicology is concerned with the investigation, management, and preven-tion of diseases arising from chemicals in the workplace. While it is primarily concerned with the health of workers exposed to toxic agents, it recognizes that their families, other household contacts, and the general public may also be affected. There may also be con-current environmental impacts.

Occupational toxicology is a subset of environmental public health that requires the close co-operation of many professional groups, including occupational physicians, occu-pational hygienists, environmental health practitioners, government inspectors, health and safety officers, toxicologists, chemists and chemical engineers, design engineers, managers, trade union representatives, information scientists, and the workers them-selves (Figure 8.1 ). Occupational toxicologists provide the other professionals with vital understanding of the nature of toxic agents and hazards, to enable the assessment and management of risks, and appropriate responses to chemical exposures and incidents.

The UK’s Health and Safety at Work (etc) Act 1974 (HASAWA) is the primary piece of legislation covering health and safety in the UK. The Act established the Health and Safety

Commission (HSC) and its operating arm, the Health and Safety Executive (HSE). In 2008, the HSC and HSE merged, bringing together their powers and functions, and retaining the name Health and Safety Executive . The HASAWA and related legislation, such as the Health and Safety (Offences) Act 2008, is enforced by the HSE or, in certain cases, mainly relating to distribution, retail, leisure, and catering sectors, by local author-ities. The Act recognizes the pluralistic approach and places general duties regarding health and safety on all people at work (except domestic servants), including employers, the self-employed, and employees, as well as the HSE itself.

8.2

History of occupational diseases

Occupational toxicology is not new. The Romans recognized that certain occupations were associated with particular diseases. The first such textbook is attributed to Bernardino Ramazzini (1633–1714), who worked as a physician and professor in Padua and Modena, Italy. In 1713 he published De morbis artificum diatriba (An account of the diseases of work; Ramazzini 1713 ), in which he described over 50 occupational disorders, along with an account of working conditions at the time:

◆ occupational asthma in grain workers;

◆ pneumoconiosis and other diseases of miners;

Government

Work environment

Work environment

Management Worker

Safety team Safety improvement

Technology

Economics Customer

Fig. 8.1 Occupational toxicology is a subset of environmental public health that requires the close co-operation of many professional groups and the workers themselves. Adapted from the University of New South Wales, School of Safety Science, 2008.

◆ lead poisoning in potters;

◆ silicosis in stonemasons;

◆ diseases among metal workers and of gilders and printers;

◆ workers who cleaned out the city cesspits developed eye infections, which lead to sight loss or total blindness;

◆ breast cancer occurred more often in nuns than in other women of similar age.

Ramazzini methodically collected data relating to diseases of manual workers in relation to their occupation. In the same way today, when a disease is shown to be more prevalent in a particular group of workers than it is in the general population, it is suggestive of an occupational disease.

8.3

Types of adverse effects

Chemical exposure in the occupational setting can cause a wide range of effects if appropri-ate controls are not in place. These will depend on various factors, including the exposure route, duration and dose, and the frequency of exposure as well as the individual exposed and any pre-existing diseases or susceptibilities. The effects may be acute or chronic or even delayed, with a long lead time between exposure and disease. This is particularly important with cancer-causing chemicals. Issues relating to fertility and effects on the foetus and the growing child from parental chemical exposure should also be of concern.

In this chapter, two examples of adverse effects from the occupational use of chemicals are provided. The first describes the acute effects of chlorine and the second describes the acute but, more significantly, the chronic effects of vinyl chloride monomer (VCM).

8.3.1 Chlorine: health effects of acute/single exposure

In a properly managed safe system of work, acute exposure to chlorine will not occur.

However, should there be an incident in which there is a release the immediate symptoms following inhalation of chlorine include a burning sensation in the eyes and nose, sore throat, cough, chest tightness, headache, fever, wheeze, fast heart rate, and confusion.

Sufficient exposure may induce reflex cholinergic bronchoconstriction, with associated signs of coughing, wheezing, and dyspnoea (HPA 2011 ). Exposure to a sufficiently high dose may result in pulmonary oedema and respiratory failure, the onset of which may be delayed by up to 36 hours. There is some evidence to suggest that exposure to chlorine may be associated with long-term neuropsychological changes (Dilks and Matzenbacher 2003 ), although further studies are required to confirm this hypothesis. A summary of the acute effects of chlorine exposure by concentration is given in Table 8.1 .

8.3.1.1 Delayed effects following an acute exposure

Most studies of survivors of World War I gassing incidents have reported a high incidence of acute respiratory damage and a lower incidence of chronic sequelae following acute exposure (Ayres and Baxter 2004 ). Similar sequelae have also been reported for individuals following acute exposure to the accidental release of chlorine gas, with the most consistently reported chronic effect being a reduction in the forced expiratory volume (FEV) (IPCS 1999a ).

A relatively recent report relating to accidental exposure to chlorine gas suggests that chronic sequelae following acute exposure may be more frequent than previously anticipated: a fol-low-up study in July 1999 on 20 individuals (previously exposed in 1995) indicated that 75 % had residual lung volumes below 80 % of their predicted value and nearly half the subjects tested for airway reactivity to methacholine had a greater than 15 % decline in FEV (Schwartz et al. 1990 ). There is some evidence to suggest that a single, acute exposure to chlorine gas may cause reactive airways dysfunction syndrome (RADS), also known as irritant-induced asthma (Ayres and Baxter 2004 ; Winder 2001 ).

8.3.2 Vinyl chloride: exposure and health effects

Vinyl chloride (Figure 8.2 ), which is produced for industrial use as a chemical intermedi-ate in the manufacture of other compounds, particularly polyvinyl chloride (PVC), is toxic by all routes of exposure. It is metabolized to the active metabolites chloroethylene oxide and chloracetaldehyde, which is responsible for its toxicity. In the absence of prop-er controls, acute exposure will produce immediate signs and symptoms, such as respira-tory irritation, producing coughing, wheezing, and breathlessness following inhalation, and also systemic effects, including headache, ataxia, drowsiness, and coma. In addition, some halogenated hydrocarbons can cause cardiac arrhythmias (IPCS 1999b ; NPIS 2004 ).

Ingestion of vinyl chloride may cause sickness, diarrhoea, and stomach pain. Contact of the skin or eyes with vinyl chloride liquid or vapour could cause irritation and dermatitis.

Exposure to escaping gas from compressed (liquid) vinyl chloride may cause frostbite (HPA 2008 ).

Table 8.1 Summary of acute toxic effects in relation to approximate (air) concentration of chlorine (IPCS 1996)

Concentration Signs and symptoms

ppm mg/m³

1–3 3–10 Mild mucous membrane irritation.

5–15 15–45 Moderate irritation of upper respiratory tract.

30 90 Immediate chest pain, vomiting, coughing.

40–60 115–175 Toxic pneumonitis and pulmonary oedema.

430 1250 Lethal after 30 minutes exposure.

1000 2900 Lethal in minutes.

Concentrations (mg/m ³ ) are approximate conversions from the corresponding ppm value.

Data from IPCS (1996) Chlorine. International Programme on Chemical Safety Poisons Information Monograph PIM 947. Available at http://www.inchem.org/documents/pims/chemical/pim947.htm (accessed 17.08.11)

H H

Cl H C C

Fig. 8.2 Vinyl chloride monomer.

Where there are inadequate controls, long-term exposure may cause impotence, blood disorders, liver problems (angiosarcoma), and the pathopnemonic disease of acroosteolysis following adult exposure to vinyl chloride. Bone loss in the fingertips due to exposure to VCM has been observed among polyvinyl chloride (PVC) reactor workers (NIOSH 2001 ).

The term ‘acroosteolysis’ was used to name the condition (the word ‘acroosteolysis’ is derived from Greek words akron = extremity, osteon = bone, lysis = dissolution) and has been defined as a shortening of the terminal digits.

A Department for Work and Pensions ( 2005 ) review concluded that there was consist-ent evidence that the inhalation of VCM in PVC production workers causes a character-istic clinical triad of osteolysis of the terminal phalanges, scleroderma, and Raynaud’s phenomenon, but not all three are invariably present together (Department for Work and Pensions 2005 ). These effects occurred in workers who had been exposed to levels of VCM very much higher than the current control limits. Surveys of factory workforces have shown that among those exposed to VCM who do not have radiological evidence of osteolysis, the prevalence of Raynaud’s phenomenon and scleroderma is greater than in the general population (by a factor of two).

The mechanisms of toxicity for non-cancer VCM effects are not completely elucidated.

VCM disease exhibits many characteristics of autoimmune diseases (e.g. Raynaud’s phe-nomenon and scleroderma). B-cell proliferation, hyperimmunoglobulinemia, and com-plement activation, with increased circulating immune complexes or cryoglobulinemia indicating stimulation of immune response, have been observed.

Postulated mechanisms for the non-cancer effects include:

1. Immunological

◆ a reactive vinyl chloride intermediate metabolite, such as 2-chloroethylene oxide or 2-chloroacetaldehyde, binds to a protein such as IgG;

◆ altered protein initiates an immune response, with deposition of immune products along vascular endothelium;

◆ circulating immune complexes are proposed to precipitate in response to exposure to the cold, and these precipitates are proposed to produce blockage of the small vessels.

2. Resorptive bone changes in the fingers may be due to activation of osteoclast second-ary to vascular insufficiency in the fingertips (ATSDR 2006 ).

However, the International Agency for Research on Cancer has classified vinyl chloride as a known human carcinogen, based on evidence of carcinogenicity in both humans and animals (IARC 1987 ). It is mutagenic and its carcinogenic action is believed to occur via a genotoxic mechanism. VCM is covered by the Carcinogens Directive, and the current workplace exposure limit of 3 ppm is based on its recognized carcinogenicity rather than non-cancer endpoints.

8.4

Assessing occupational disease and hazardous chemicals

It is important to recognize that occupational diseases are preventable by adopting appropri-ate control measures, yet they can be responsible for temporary and permanent disablement,

discomfort, and distress, as well as lost productivity. The risks extend to co-workers, the worker’s family, and the environment. Occupational hygienists stress the importance of anticipation and prevention before a system of work is introduced.

Diseases can have occupational and non-occupational causes. Occupational causes may be overlooked if the patient presents outside the occupational health sector (Figure 8.3 ).

Occupational illnesses may resemble non-occupational illnesses, and a very long latency period can sometimes exist between exposure and the emergence of signs and symptoms.

There are thousands of jobs, chemicals, and diseases, and an association may not be readily apparent. In addition, medical students and most other health professionals are not trained in occupational toxicology.

Occupational disease can be identified by consideration of health data , i.e. epidemiological studies, health assessments, the incidence of particular diseases in a workforce, or the appear-ance of signs and symptoms in individual workers or their families, together with knowledge of the chemicals in the workplace, the available data on their toxicity, risk assessment, and monitoring. In most cases, risk assessment will be based on the available toxicology data (largely from experimental studies in animals) together with estimates of exposure.

An investigation into suspected ill-health from workplace exposure to a hazardous chem-ical will start with an analysis of the system of work, to identify which chemchem-icals are used in which locations by which workers and consideration of the data on their toxicity. The source-pathway-receptor model is a useful starting point. The exact activities, times, and durations should be recorded. Existing risk assessment documentation and inventories should provide information to identify critical control points, but they must be assessed critically.

Investigations may involve biological/clinical sampling to detect and measure the pres-ence of the toxic agent or its metabolic products in body tissue or excreta — typically blood, urine, or exhalation samples. In some cases it may be necessary for medical exami-nation of the exposed workers and specific organ-function tests. Clearly there are practical and ethical issues here, including consent and confidentiality, not to mention the possibility

Diseases (Epidemiology)

Chemicals (via occupational hygiene and risk assessment)

Occupational disease

Hazardous chemicals

Hazardous job tasks

Industries

Occupations

Industrial processes

Chemical exposure at home and in

the non-work environment

Fig. 8.3 Ways of identifying occupational toxicity-related diseases.

of personal distress, and industrial relations problems. These will need careful handling and good communications.

Environmental sampling may be carried out to provide data for an exposure assess-ment. This may involve air and dust sampling. In some hazardous situations there may already be continuous monitoring data. The sampling strategy should be appropriate to the pattern of work and activities of individual workers, and their locus and exposure to the particular hazardous chemicals.

Environmental and/or biological sampling data must be complemented by taking the work history, present and past, of the affected individuals, including the type of work and its physical and psychological demands, detailed accounts of working practices, including exposures to physical, chemical, or biological hazards, and the control measures employed (e.g. PPE) should be recorded. This should not be confined to the worker’s current work activity and employer, but should if possible cover their entire working lives.

Particular attention should be paid to whether there have been any recent changes in work-ing practices, materials employed, or workplace control mechanisms. Absenteeism, sickness leave, and employee turnover records should be analysed. Analysis and evaluation will lead to recommendations for risk management control measures (see section 8.5 in this chapter).

8.4.1 Multi-exposure to hazardous chemicals

It must be remembered that in the modern workplace it is unlikely that a worker will be exposed to only one hazardous chemical. Multiexposure issues of interactions between substances include:

◆ independent — no cross reaction between the compounds, e.g. carbon monoxide and cadmium;

◆ antagonistic — exposure protects against the production of toxicity, e.g. antidotes;

◆ potentiative — the single compound has no effect unless other is present, e.g. carbon tetrachloride and 2-propanol;

◆ additive — effect is additive in nature, e.g. solvents;

◆ synergistic — effect is multiplicative, e.g. asbestos and smoking.

8.5

Risk management

The exposure of workers to hazardous chemicals must be prevented or adequately con-trolled. The UK Control of Substances Hazardous to Health Regulations (COSHH) (see section 8.6 below) make risk assessment and risk management mandatory.

A hierarchy of control measures is given below. Elimination and substitution should always be considered first, whether as long-term or short-term solutions, before the use of engineering controls. It should be noted that the use of PPE is a final resort after all other controls have been implemented.

◆ Elimination of hazardous chemical

◆ Substitution with less hazardous materials or forms of the material (e.g. pellets instead of powder) or processes.

◆ Minimization of inventories or stocks or amounts of available hazards.

◆ Engineering controls at source, such as automation or process enclosure.

◆ Engineering controls to reduce exposure, such as segregation, partial enclosure, mechanical handling, suppression methods, or ventilation.

◆ Administrative controls, such as safe working procedures, job rotation, good house-keeping.

◆ Reduction of the number of workers exposed.

◆ Personnel procedures, such as adequate supervision, information dissemination, and training.

◆ Health surveillance.

◆ Personal protective equipment.

COSHH impose special controls over carcinogens. The concept of substitution is encouraged, which is the second most effective measure in the hierarchy of control measures.

Table 8.2 provides recommendations for substitution of materials.

8.6

Legal controls and standards

The COSHH made under HASAWA, apply to substances or mixtures of substances classified as dangerous to health under the Chemicals (Hazard Information and Packing for Supply) (CHIP) Regulations. CHIP requires the supplier of a dangerous chemical to identify the dan-gers associated with the chemical, which is known as ‘classification’, give information about the hazards to their customers, usually through labelling, and package the chemical safely.

In addition, under the European Union regulations on Registration, Evaluation, Authorisation and restriction of Chemicals (REACH) suppliers are required to provide safety data sheets for their products. COSHH require a risk assessment to be carried out and control measures to be implemented to prevent or control exposure. Control measures

Table 8.2 Substitution: some examples Examples of Chemical Substitution

Instead of: Consider:

Carbon tetrachloride 1,1,1,-Trichloroethane

Benzene Toluene, Cyclohexane, Ketones

Lead Lead-free solders

Lead-free paints Organic solvents Water-based solvents

Liquid carbon dioxide Sandstone grinding

wheels (silica)

Synthetic grinding wheels such as aluminum oxide

Examples of Chemical Substitution. Accessed 0-662-38542-X; H46-2/04-373E http://www.hc-sc.gc.ca/ewh-semt/

occup-travail/whmis-simdut/substitution-eng.php, 2006. Reproduced with the permission of the Minister of Public Works and Government Services Canada, 2012.

may include the monitoring of the exposure of workers and appropriate health surveillance.

Workers must be properly trained and supervised, and control measures must be properly maintained and implemented. Occupational exposure limits have been set (see section 8.7 below) and these are found in the HSE publication EH40.

In 2005, existing requirements to follow good practice were brought together by the introduction of eight principles as an update to the Control of Substances Hazardous to Health (Amendment) Regulations 2004 (Box 8.1 ).

Basic advice on the implementation of the COSHH regulations is also provided on the HSE website COSHH Essentials.

8.7

Occupational exposure limits

8.7.1 Workplace exposure limits

Workplace exposure limits (WEL) have now replaced maximum exposure limits (MELs) and occupational exposure standards (OESs) in the UK. Many of the old MELs and OESs have been converted to WELs, apart from about 100 OESs that have been deleted. There are no WELs for asbestos, lead and other substances that have specific legislative controls.

The list of exposure limits is known as EH40 and is available from the HSE Direct website.

Readers are advised to familiarize themselves with HSE COSHH guidance publications, including EH40 ( www.hse.gov.uk ).

Box 8.1 Principles of good practice for the control of

In document Doctorado en Ciencias de la Educación (página 63-79)