Forensic issues arising in the assessment of chlorine-related deaths in a domestic setting

Abstract

A retrospective review of autopsy files at the Forensic Science South Australia, Australia, was undertaken over a 20-year period from January 2000 to December 2019 for all cases where chlorine had caused or contributed to death. Two cases were identified out of a total of 25,121 autopsies (0.008%): a 53-year-old man who committed suicide in a cellar with granulated chlorine, and a 49-year-old woman with asthma who died of acute bronchospasm due to exposure to chlorine gas while mixing swimming pool chemicals in her kitchen. Chlorine-related deaths are uncommon in domestic situations. However, the absence of biomarkers and non-specific findings at autopsy complicate the diagnosis, particularly as environmental levels are not stable. While accidents with cleaning agents or swimming pool reagents are the most common event in the literature in domestic settings (exclusive of industrial or transportation accidents), suicide may also very rarely occur. Individuals with asthma and chronic respiratory diseases are at higher risk of an adverse outcome upon exposure to chlorine gas, with inattention to proper storage conditions and handling protocols being additional risk factors.

Keywords

Chlorine poisoning toxicity death inhalant swimming pool

Introduction

Chlorine is a greenish-yellow, non-combustible, toxic gas that may cause significant pulmonary irritation. It was discovered in 1774 and was first used to bleach textiles. Serious injuries and deaths have occurred associated with industrial accidents and during a number of wars when it was used as a chemical weapon. Chlorine has multiple industrial uses but is also commonly employed as a disinfecting agent for homes and swimming pools.¹ The mechanism of its toxicity results from its partial solubility in water causing it to dissolve into fluid lining the airways, leading to the formation of hypochlorous acid and hydrochloric acid.^1,2 These in turn cause epithelial damage, most likely due to direct oxidative injury with a subsequent inflammatory response and release of oxidants and proteolytic enzymes mediated by transient receptor potential channels.^3,4

While military uses of chlorine and industrial accidents have resulted in multiple casualties, fatalities due to chlorine inhalation in domestic settings are rare. The non-specific nature of autopsy findings and the difficulties in chemical analyses may both contribute to problems in establishing diagnoses. To illustrate these issues, the following study was undertaken.

Methods

A retrospective study was undertaken of autopsy cases at the Forensic Science South Australia (FSSA), Australia, state mortuary over a 20-year period from January 2000 to December 2019 for all cases where chlorine was mentioned as a cause of or contributor to death. From the de-identified autopsy information, the age, sex, cause and mechanism of death, and circumstances were reviewed.

Results

Two cases were identified out of a total of 25,121 autopsies (0.008%): a 53-year-old male and a 49-year-old female.

Case 1

A 53-year-old man was found dead inside a shed cellar with his golden retriever dog (also deceased). A variety of tools and a trestle table were piled against the cellar door. There was a strong smell of chlorine within the shed and cellar. Attending Metropolitan Fire Service officers reported that there were granules of chlorine on the floor of the cellar with atmospheric readings which showed a chlorine concentration of 0.2 parts per million (ppm) after the cellar had been opened for some time and the decedent and his dog removed. No other poisons, toxins or drugs were detected. There was no significant past medical history.

At autopsy, the body was that of an adult white male (body mass index (BMI) 25.1 kg/m²). External examination revealed occasional scattered minor bruises and abrasions on the extremities. Internal examination showed marked congestion and oedema of the lungs (combined weight 1578 g) with bilateral reddish pleural effusions. The other organs and structures were unremarkable. Histology confirmed pulmonary congestion and oedema with focal intra-alveolar haemorrhage. Toxicological screening was negative for common drugs and alcohol. Chlorine testing is not available at FSSA.

As there was no significant trauma and no underlying organic diseases which could have caused or contributed to the lethal episode, the cause of death was attributed to chlorine inhalation, manner suicide.

Case 2

A 49-year-old woman who was mixing swimming pool chemicals in the kitchen sink at her home address called out to her daughter for her asthma nebuliser. The daughter noted that she was choking, coughing and expectorating. Her mother informed her that the container of pool chemical had ‘exploded’ when she opened it. She attempted to wash the chemicals off in the shower but kept choking and was unable to tolerate the mask of her nebuliser. She then collapsed, stopped breathing and became pulseless. Resuscitation attempts by ambulance personnel were not successful. Her medical history included asthma and chronic obstructive pulmonary disease.

Attending police officers noted a strong smell of chlorine in the kitchen with splashes of damp pool chemical in and around the sink. There was no evidence of an explosion, and a closed container of dry pool chemical (granular chlorine, active ingredient calcium hypochlorite) was present on the adjacent kitchen table.

At autopsy, the body was that of an adult white female (BMI 32.9 kg/m²). External examination revealed no abnormalities, with the internal examination showing congestion of the laryngeal, tracheal and bronchial mucosa with focal areas of submucosal haemorrhage. There was also marked congestion and oedema of the lungs (combined weight 1164 g). Other findings included moderate coronary artery atherosclerosis, with no evidence of old or recent myocardial infarction, mild steatosis of the liver and incidental gallstones. Histological examination of the lungs showed emphysematous changes with congestion and oedema as well as goblet cell hyperplasia, basement membrane thickening, bronchial smooth-muscle thickening and submucosal infiltrates of eosinophils in keeping with the history of asthma. There was no evidence of pneumonia, aspiration or pulmonary thromboembolism. Toxicological screening was negative for alcohol and common drugs (other than those associated with attempted resuscitation). As noted above, chlorine testing is not available at FSSA.

As there was no significant trauma and no other underlying organic diseases which could have caused or contributed to the lethal episode, death was attributed to acute bronchospasm due to exposure to chlorine gas, manner accident.

Discussion

Inhalation of gases other than oxygen may result in lethal outcomes by a variety of mechanisms. For example, inert gases such as nitrogen, helium, propane and methane can cause death by simply replacing oxygen, leading to asphyxiation.^5–8 Carbon monoxide operates somewhat differently by displacing oxygen from haemoglobin and also by causing toxicity at a cellular level.⁹ These exposures can be accidental or self-inflicted. Chlorine is heavier than air – a fact which would have facilitated death in case 1 by displacing air from the underground cellar.

Chlorine gas was first used as a major chemical weapon during the Second Battle of Ypres on 22 April 1915 in the First World War when German troops released 150 tons of gas from 6000 gas cylinders, causing 5000 fatalities.¹⁰ The death rate from exposure was approximately 5%, and by the end of the war, there were approximately 1.3 million victims of gas attacks.⁴ Despite being prohibited by the Geneva Protocol of the League of Nations in 1925, nine attacks occurred during the Iraq War between 2007 and 2009, and it was used on larger scale in the Syrian Civil War.^4,11

In the USA, 13–14 million tons of chlorine are produced annually, much of which is transported cross-country by rail. A train derailment in 2005 in Graniteville, South Carolina, which released 42–60 tons of chlorine gas demonstrated the potential vulnerability of railway towns, with nine deaths, 71 hospitalisations and 525 outpatient treatments.^11,12 The potential for chlorine to be used as a terrorist weapon is therefore significant, with more than 17,000 deaths and 100,000 injuries predicted to occur if gas was intentionally released in a high population density area in the USA.¹³

Chlorine acts by causing irritation along the entire length of the airway from the nasal passages to the alveoli, resulting in a spectrum of conditions ranging from reactive airways dysfunctional syndrome to adult respiratory distress syndrome and, on occasion, acute lung injury and death.³ The clinical response depends on the concentration of gas and the duration of exposure.¹⁴ At 1–3 ppm, mucus membranes become irritated which progresses to shortness of breath, coughing and retrosternal chest pain when levels exceed 30 ppm. Concentrations above 400 ppm usually cause death within 30 minutes, with levels above 1000 ppm resulting in death within minutes.³ Glottic oedema and laryngospasm may also be acutely life threatening.⁴ Survivors may develop restrictive lung disease due to chronic inflammation and pulmonary fibrosis.¹⁵ Chlorine may also injure the systemic vasculature by damaging endothelial cells and depressing myocardial activity, leading to cardiac failure.¹⁶ At higher doses, it has had neurotoxic effects in animal studies, causing ataxia, tremors and seizures.¹⁰ The death rate from civilian exposure is approximately 0.6%.⁴ Although cardiomegaly has been noted at autopsy in lethal cases, it is unclear whether this is due to pre-existing cardiac disease or the effect of acute pulmonary hypertension.¹⁷

Asthma is known to increase adverse responses to chlorine inhalation,³ as was observed in case 2. The relationship between chlorine and asthma is, however, something of a vicious cycle, as it has been demonstrated that elite swimmers have a higher incidence of respiratory symptoms, airway inflammation and asthma that has been attributed to long-term exposure to pool chlorine.¹⁸ This finding has been supported in a study of adolescent recreational pool users which found that the cumulative time of chlorinated pool exposure was significantly associated with the development of allergic rhinitis, hay fever and asthma.¹⁹

In a domestic setting, exposure to chlorine most often occurs from routine use of swimming pools, on occasions when pool systems have malfunctioned or when domestic cleaners have been misused and bleach has been mixed with acid. An analysis of 1566 cases of civilians exposed to chlorine showed that the majority – 1097 (70%) cases – were industrial or transportation accidents, 425 (27%) cases involved swimming pools and only 44 (3%) cases had been caused by reactions involving cleaning agents.¹⁷ However, in 2018, the American Association of Poison Control Centers estimated that approximately 35% of the exposures were caused by mixing bleach (hypochlorite) with household acid.²⁰

The release of chlorine in case 2 is most likely related to inadequate storage and handling. Calcium hypochlorite gradually decomposes to produce chlorine gas, and so it is possible that a build-up of chlorine gas in the container was released upon opening. Manufacturers’ instructions also specify that pool chemicals should be stored in ‘breathable’ containers to avoid pressure build-up while in storage and that pool chemicals should only be added in small amounts to large volumes of water rather than the reverse. Adding a limited amount of water to a dry chemical may also result in an increase in temperature and the release of chlorine gas. It is also specified that the product should only be used outdoors or in well-ventilated areas.

The reported cases demonstrate the relative rarity of chlorine-related deaths in domestic situations removed from industrial and transportation accidents. The absence of biomarkers and the non-specific findings at autopsy may complicate the diagnosis, particularly as environmental levels are not stable.⁴ While accidents with cleaning agents or swimming pool reagents are the most common event in domestic settings, suicide, as was demonstrated in case, 1 may also very rarely occur. Individuals with asthma and chronic respiratory diseases are at higher risk of an adverse outcome upon exposure to chlorine gas, with inattention to proper storage conditions and handling protocols predisposing them to inadvertent exposure, as occurred in case 2.

Footnotes

Declaration of conflicting interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

ORCID iD

Roger W Byard

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