An African soldier is advancing an occupational disease claim against the Ministry of Defence (MoD), valued at £150,000.[i]
Incidentally, last month, the Defence and Security Accelerator (DASA) allotted £1 million to fund 6 month trials and demonstrations of new wearable technology which are designed to reduce the risk of musculoskeletal injury (MSKI), environmental injury (heat and cold) and noise-induced hearing loss (NIHL).[ii]
The 36-year-old claimant, who served with the Adjutant General’s Corps, argues that he suffered a non-freezing cold injury (NFCI) as a result of the British Military’s failure to protect him from cold climate conditions.
In edition 188 (here), our feature article on work in cold temperatures included information on military claims for NFCI, which typically result from bodily extremities enduring cold and wet conditions for a prolonged period of time.[iii]
The MoD maintains that negligence liability, in relation to the most recent claim, is contested.
Mr Asiamah, who was born in Ghana, alleges that his cold-related injury developed during training exercises conducted in Leicester, UK, in March 2016. After attending 2 days of battlefield training within the space of 1 fortnight (a combined period of 18 hours), the claimant asserts that he began to suffer numbness and pain in his hands and feet. He was provisionally diagnosed with NFCI, after which he was recommended for downgrading and protection from the cold.
It is his pleaded case that his ethnicity made him more susceptible to the cold weather conditions faced in the course of his employment and that this predisposition was common knowledge to his employers and was therefore foreseeable. He cites Burgess and Macfarlane (2009), whose study concluded that:
‘Young male African Americans in the British Army are at 30 times greater chance of developing peripheral cold injury and are more severely affected than their Caucasian counterparts following similar climatic exposure, using similar clothing and equipment’.[iv]
8 months post-onset of injury, Mr Asiamah left the Army, on albeit unrelated grounds. As a consequence of his condition, he avers that he is still at risk of aggravating his symptoms if he leaves his home in temperatures below 15°C.
In respect of breach of duty, he argues that the MoD was negligent, as they did not warn him to bring gloves, winter socks and boots to the training exercises. However, military officials state that appropriate ‘clothing, equipment and training’ was supplied to the claimant and reject any assertion that a risk assessment should have been undertaken.
What is more, the claimant argues that he was told to ‘carry on’ working after colleagues were first made aware of his cold injury symptoms. Under MoD protocol, NFCI sufferers must be evacuated immediately to receive the necessary medical attention.[v]
Literature on Ethnicity and NFCI Vulnerability
Ordinarily, exposure to wet cold of 10° C for 10 hours is a rough guideline threshold of exposure, but the threshold for NFCI is variable.[vi]
In several studies, the effect of ethnicity on NFCI incidence has been investigated. Nagarijan (2015)[vii] reached similar conclusions to the 2009 paper adduced by Mr Asiamah, while De Kruijf (2016) detected a small reduction in cold detection sensitivity in those with black skin.[viii] Moreover, DeGroot (2003) and Candler (1997) calculated that male African soldiers were 3.7 and 3.9 times more likely, respectively, to suffer ‘cold weather injury’.[ix] [x] These are less significant associations than the 2009 study and refer to freezing cold injury (FCI) in conjunction with NFCI, but are still statistically significant. Tek (1993), by contrast, did not consider that black skin pigmentation was an indicator of individual NFCI risk.[xi]
In a Ministry of Defence document, entitled Synopsis of Causation (2008), the medical practitioner authors validate the general expert consensus that ethnicity plays a role in the onset of NFCI, citing DeGroot (2003) and Candler (1997) as authority:
However, an unclassified US Army Research Institute paper acknowledged this as far back as 1989:
‘Blacks demonstrate greater cold sensitivity than Caucasians and, therefore, are at greater risk for peripheral vascular cold injury’.[xii]
In previous claims brought against the MoD, it has been submitted that the British military has had access to research, dating back to 1984, which states that black army personnel have ‘a 2.8 to sixfold increased likelihood of developing symptoms’ of NFCI. This discovery was in relation to black paratroopers who fought in the Falklands war.[xiii]
The scientific reasoning underpinning increased vulnerability to cold is not definitively accepted among experts:[xiv]
- Chung (2019), Daanen (2003) and Eglin (2013) have suggested that the physiological pathway for heightened susceptibility could be reduced cold-induced vasodilation (a cyclic oscillation in blood flow on cold exposure that commonly occurs in the extremities[xv]) in African individuals.[xvi]
- Similarly, Maley (2014) identified that Africans had a higher skin temperature threshold for both the initiation of vasoconstriction and vasodilatation, along with a lower skin blood flow and a slower rate of rewarming.[xvii] This has been an established topic of research since the 1950’s.[xviii] [xix]
- Whereas Kim et al. (2006) proposed that the biological mechanism could be due to genetic variation in sensory receptors which monitor heat and cold sensation; this may follow a pattern of ethnicity.[xx]
- Alternatively, Polydefkis et al. (2006) considered that African populations may reproduce sensory neurons at a slower rate, i.e. slower nerve regeneration.[xxi]
[i] Cyril Dixon, ‘African soldier sues the Army for 'failing to protect' him from British cold’ (27 December 2018 The Daily Express) <https://www.express.co.uk/news/uk/1064149/african-soldier-british-army-failing-to-protect-britain-cold> accessed 7 January 2019.
[ii] Defence and Security Accelerator, ‘Wearable technology for injury prevention’ (17 December 2018 GOV.UK) <https://www.gov.uk/government/news/wearable-technology-for-injury-prevention> accessed 9 January 2019.
[iii] Deniz Tek, MBBS and Steven Mackey, MD. Non-freezing cold injury in a Marine infantry
Battalion. Journal of Wilderness Medicine 1993; 4: 353-357 <https://www.wemjournal.org/article/S0953-9859(93)71202-4/pdf> accessed 8 January 2018.
[iv] Burgess JE, Macfarlane F. ‘Retrospective Analysis of the Ethnic Origins of Male British Army Soldiers with Peripheral Cold Weather Injury’ Journal of the Royal Army Medical Corps 2009; 155:11-15 <https://jramc.bmj.com/content/155/1/11> accessed 7 January 2018.
[v] JSP 539 HEAT ILLNESS AND COLD INJURY: PREVENTION AND MANAGEMENT Part 2: Guidance (May 2017 Ministry of Defence) <https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/611846/20170427_JSP_539_Part_2_V3.pdf> accessed 7 January 2019.
[vi] Shaw, J. Frostbite. In: Rosen, P., Baker, F., Barkin, R., Braen, G., Dailey, R. and Levy, R. ed.
Emergency Medicine. Concepts and Clinical Practice. St Louis: Mosby, 1988: 610.
[vii] Nagarajan S . Update: cold weather injuries, active and reserve components, U.S. Armed Forces, July 2010-June 2015. MSMR 2015; 22: 7–12. <https://www.ncbi.nlm.nih.gov/pubmed/26505075> accessed 8 January 2019.
[viii] de Kruijf M , Peters MJ, C. Jacobs L, Tiemeier H, Nijsten T, Hofman A, et al. Determinants for quantitative sensory testing and the association with chronic musculoskeletal pain in the general elderly population. Pain Pract 2016; 16: 831–41. <https://www.ncbi.nlm.nih.gov/pubmed/26205731> accessed 8 January 2019.
[ix] DeGroot DW, Castellani JW, Williams JO, Amoroso PJ. Epidemiology of U.S. Army cold weather injuries, 1980–1999. Aviat Space Environ Med. 2003;74:564–570. <https://www.ncbi.nlm.nih.gov/pubmed/12751587> accessed 8 January 2019.
[xi] Ibid at 3.
[xii] Jackson RL, Roberts DE, Cote RA, McNeal P, Fay JT, Sharp MW, Kraus E, Rahman SA, Hamlet MP. Psychological and Physiological Responses of Blacks and Caucasians to Hand Cooling. Report No: T20-89. Natick: US Army Research Institute of Environmental Medicine; 1989 <https://apps.dtic.mil/dtic/tr/fulltext/u2/a215646.pdf> accessed 8 January 2019.
[xiii] Tom Batchelor, ‘Black soldier sues MoD over ethnicity claim after sustaining injury during -30C drill’ (18 April 2016 The Daily Express) <https://www.express.co.uk/news/uk/662062/Black-soldier-sues-MoD-ethnicity-claim-sustaining-injury-30C-drill> accessed 8 January 2019.
[xiv] Tom A Vale, Mkael Symmonds, Michael Polydefkis, Kelly Byrnes, Andrew S C Rice, Andreas C Themistocleous, David L H Bennett; Chronic non-freezing cold injury results in neuropathic pain due to a sensory neuropathy, Brain, Volume 140, Issue 10, 1 October 2017, Pages 2557–2569, <https://doi.org/10.1093/brain/awx215> accessed 8 January 2019.
[xvi] Cheung SS. Responses of the hands and feet to cold exposure. Temperature (Austin). 2015 Jan-Mar; 2(1): 105–120. <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4843861/> accessed 8 January 2019.
Daanen HA . Finger cold-induced vasodilation: a review. Eur J Appl Physiol 2003; 89: 411–26. <https://www.ncbi.nlm.nih.gov/pubmed/12712346> accessed 8 January 2019.
Eglin CM, Golden FS, Tipton MJ. Cold sensitivity test for individuals with non-freezing cold injury: the effect of prior exercise. Extreme Physiol Med 2013; 2: 16. <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3710088/> accessed 8 January 2019.
[xvii] Maley MJ The effect of ethnicity on the vascular responses to cold exposure of the extremities. Eur J Appl Physiol. 2014 Nov;114(11):2369-79. doi: 10.1007/s00421-014-2962-2. Epub 2014 Aug 1. <https://www.ncbi.nlm.nih.gov/pubmed/25081130/> accessed 8 January 2019.
[xix] Rennie D, Adams T. Comparative thermoregulatory responses of Negroes and white persons to acute cold stress. J Appl Physiol. 1957;11:201–204. <https://www.ncbi.nlm.nih.gov/pubmed/13475165> accessed 8 January 2019.
[xx] Kim H , Mittal DP, Iadarola MJ, Dionne RA. Genetic predictors for acute experimental cold and heat pain sensitivity in humans. J Med Genet 2006; 43: e40. <https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2564596/> accessed 8 January 2019.
[xxi] Polydefkis M , Sirdofsky M, Hauer P, Petty BG, Murinson B, McArthur JC. Factors influencing nerve regeneration in a trial of timcodar dimesylate. Neurology 2006; 66: 259–61. <https://www.ncbi.nlm.nih.gov/pubmed/16434669> accessed 8 January 2019.