COMMISSION
OF
INQUIRY
INTO
SAFETY
AND
HEALTH
IN
THE
MINING
INDUSTRY
50
CERTIFCATION UNDER ACT 78 OF 1973: BLACKS
LIVING
DECEASED
PERIOD CD CD+T
T/c T/a Total 1ST 2ND 2+T T
Total
10/73
-
3/74 323 578 981 192 2074 152 43 35 2 232
4/74
-
3/75 740 1055 1900 421 4116 325 55 66 6
452
4/75
-
3/76 847 1312 2293 549 5001 440 60 109 4 613
4/76
-
3/77 1077 1389 2692 508 5666 359 46 73 3
481
4/77
-
3/78 1039 1153 2795 361 5348 344 58 94 3
499
4/78
-
3/79 774 759 3042 414 4989 330 68 103 1 502
4/79
-
3/80 660 620 3071 300 4651 385 61 84 4 534
4/80
-
3/81 682 968 3175 305 5130 491 86 107 0 684
4/81
-
3/82 620 913 2978 276 4787 423 76 111 3 613
4/82
-
3/83 660 793 3273 154 4880 406 74 103 2 585
4/83
-
3/84 649 890 3424 205 5168 415 78 130 2 625
4/84
-
3/85 576 669 3217 117 4579 463 83 108 1 655
4/85
-
3/86 2282 646 3534 177 6639 414 95 119 4 632
4/86
-
3/87 2414 599 3964 152 6859 451 130 116 2 699
4/87
-
3/88 2927 606 3390 130 7053 420 97 112 2 631
4/88
-
3/89 2211 674 3678 136 6699 455 85 156 3 699
4/89
-
3/90 1215 487 3939 164 5805 277 67 126 2 472
4/90
-
12/91
4990
915
1/91
-
12/92
4628
491
99062
11014
T = TB only
Tc = TB current
T/a = TB antedated
In a period of about 20 years 128 575 mineworkers have been certified as having
acquired occupational diseases. The actual number is certainly much higher as a
result of under ascertainment among migrant labourers
who have returned to their
rural homes in any one of several labour reservoirs within South Africa or the
neighbouring States. Practically nothing is known about the fate of the persons with
certified occupational disease. A systematic study of the vital status of cases at
intervals after certification is essential if appropriate services are to be provided for
COMMISSION
OF
INQUIRY
INTO
SAFETY
AND
HEALTH
IN
THE
MINING
INDUSTRY
51
persons who have acquired disease in the course of their employment in the mines.
Though there is evidence that simple silicosis progresses very slowly, if at all, once
exposure has ceased, there is no doubt that tuberculosis
superimposed on simple
silicosis may lead to rapid deterioration, and that asbestos sets in train a progressive
disease in the absence of further exposure.
Careful scrutiny of this table may lead to a number of differing conclusions. It can
be said with confidence that it is not possible to demonstrate a consistent downward
trend in the numbers certified in any category. In addition it is clear that the number
of cases of tuberculosis certified among currently
employed black miners is
evidence of a failure of control in the mining industry and in the country as a whole.
The table does not include cases of tuberculosis in workers employed in non-risk
work. There is no information on the number of such workers, but it is reasonable to
assume that the actual total of cases is considerably larger than the official figures
suggest.
4.5.11 Evidence put before the Commission by Dr. White and Dr. Leger suggests similar
conclusions. In addition they show that although the
time between first exposure
and the diagnosis of pneumoconiosis has increased for white miners, this is not true
for black miners. This is consistent with the hypothesis that white miners in a
largely supervisory position are less exposed to dust whereas black miners in the
stopes are as heavily exposed as they were several decades ago. Elsewhere evidence
will be cited to suggest that dust levels have not changed for decades.
Evidence
from a recent study of pneumoconiosis among coal miner’s suggests that though
fewer workers are developing coal worker’s pneumoconiosis they are developing it
sooner.
The evidence demonstrates only too clearly the failure to relate dust levels to the
pattern of certification, and to identify the risk areas and the groups of workers at
risk. The absence of a systematic approach to the control
of respiratory disease
reflects the absence of appropriate analysis of available data and the long standing
fragmentation of services between distinct government departments.
4.5.12 Evidence cited by Dr. White from work done by him in the early 1980s indicated
that the death rates among South African miners from all causes or from disease had
not changed substantially between 1940 and 1980, despite the dramatic fall in both
rates between 1920 and 1940 (White Fig 1.1 p 10).
4.5.13 Estimates of the proportion of miners employed in particular tasks who will develop
pneumoconiosis still rely heavily on the original
studies carried out by Beadle, and
amplified and commented on by Du Toit, Hnizdo and King, and cited in evidence to
the Commission by White and Leger. There is general agreement that a worker in
high dust areas such as drilling, high speed development or shaft sinking for 20
years or more may face a 20 - 30% risk of developing simple silicosis. Using a
proxy
measure for risk, the length of employment of certified cases of
pneumoconiosis, it can be shown that the risk has not changed for black miners.
4.5.14 Attention was drawn to the fact that apart from the study referred to earlier, which
suggests that coal miners are developing disease sooner, there is very little
information on the risk in gold, platinum and other mines.